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Here are the best coronavirus cleaning products according to the EPA

Demand for coronavirus cleaning products remains at an all-time high. As more businesses and schools reopen, Americans are looking to clean and disinfect their offices, cars, and homes. 

To help you choose the best coronavirus cleaning products, the U.S. Environmental Protection Agency has released a list of recommended coronavirus cleaners. The list includes various household names like Lysol and Purell. Just last month the EPA updated their list adding Lysol Spray and Lysol Disinfectant Max Cover Mist to their list, which now includes over 400 cleaners. (Follow our guide on Where to Buy Lysol Spray to find the latest stock). 

Just keep in mind that these products are selling out rapidly online and in stores. (For more protection, make sure to follow or guide on where to buy face masks). 

EPA-approved coronavirus cleaning products 

Cleaning products: buy four, get one free @ Staples
For a limited time, shoppers can use coupon "98422" at Staples to get a free cleaning product when they purchase four select healthy and safety essentials. (Enter the coupon code during checkout). The sale includes hand sanitizer, Lysol Spray, Clorox Wipes, Purell, and more. View Deal

Force of Nature Kit: was $70 now $52 @ Force of Nature
Force of Nature's cleaning kit is on the EPA's list of disinfectants to use against COVID-19. It can be used on all sorts of surfaces from kitchens and bathrooms to floors and rugs. It comes with five capsules of precisely measured salt, water, and vinegar, which are converted to electrolyzed water when an electrical current changes the chemical composition of the solution into a cleaner. Use coupon "KITSAVE25" to drop its price to $52.50. View Deal

Other coronavirus cleaning products 

According to the EPA, coronaviruses are enveloped viruses, which means they are one of the easiest types of viruses to kill, as long as you're using the appropriate disinfectant. As a result, you may be wondering where to buy Clorox wipes. Fortunately, there is still stock of some of the EPA-recommended cleaners. 

In addition, the CDC says that good hygiene habits are still your best recourse. These include tips like washing your hands often with soap — for a full 20 seconds —  avoiding close contact with people who are sick, and not touching your eyes, nose, or mouth. 

As deals editor at Tom’s Guide, Louis is constantly looking for ways to avoid paying full price for the latest gadgets. That means price checking against multiple retailers and searching high and low for the best deals to bring readers. A born-and-bred New Yorker, Louis is also an avid swimmer and marathoner. His work has appeared on Gizmodo, CNET, and Time Out New York.


Force of Nature Disinfectant

This page contains affiliate links, which means that if you click on the affiliate link and buy an item, I’ll receive commissions.

There is a difference between disinfectants and cleaners.  Cleaners are designed to remove dirt and germs.  Disinfectants are supposed to kill germs.  By nature, disinfectants can’t be benign because they are killers.  Some are safe than others though.

Most disinfectants work on clean and non-porous surfaces.  And the surface has to remain wet for a certain period of time.  Read the instructions.

Force of Nature is a disinfectant and should be used accordingly.  I don’t recommend using it as an everyday cleaner.  Among other things, growing up in a sterile environment is linked to autoimmune disorders.

Force of Nature ingredients are hypochlorous acid and 0.0000003% sodium hydroxide.

In a way, hypochlorous acid (HOCl) is a form of chlorine. It’s also called electrolyzed water. During electrolysis of the solution of vinegar, salt, and water, hypochlorous acid (electrolyzed water) forms.  For your reference, the chemical name of common household chlorine bleach is sodium hypochlorite (NaClO).

The concentration of chlorine present in electrolyzed water is usually over 10 thousand times less than in household bleach.  To be on the safe side, Force of Nature states that “Those individually allergic to chlorine should avoid direct contact as it may cause irritation with symptoms of redness, itching, and swelling.”

In medical settings, hypochlorous acid is safe enough to be commonly used on open wounds and people’s faces.  You can read more about that here and here.

Hypochlorous acid is one of the most effective disinfectants for the reduction and removal of foodborne pathogens. The EPA lists one hypochlorous acid-based disinfectant (called Costeuau) in the list of COVID-19 approved disinfectants. It says that the surface has to remain wet for 10 minutes.

Force of Nature is registered with the EPA as a disinfectant. And on March 26, 2020, it was added to the EPA list for approved disinfectants for use against COVID-19.

In conclusion, I believe that it is one of the safest and effective disinfectants.

Force of Nature has given us the discount code SUMMERSTAY30  for 30% off + free shipping on Starter Kits and Bundles, valid through August 31, 2021.

Categories: COVID Preparedness, Healthy Cleaning

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Blood n-3 fatty acid levels and total and cause-specific mortality from 17 prospective studies


The health effects of omega-3 fatty acids have been controversial. Here we report the results of a de novo pooled analysis conducted with data from 17 prospective cohort studies examining the associations between blood omega-3 fatty acid levels and risk for all-cause mortality. Over a median of 16 years of follow-up, 15,720 deaths occurred among 42,466 individuals. We found that, after multivariable adjustment for relevant risk factors, risk for death from all causes was significantly lower (by 15–18%, at least p < 0.003) in the highest vs the lowest quintile for circulating long chain (20–22 carbon) omega-3 fatty acids (eicosapentaenoic, docosapentaenoic, and docosahexaenoic acids). Similar relationships were seen for death from cardiovascular disease, cancer and other causes. No associations were seen with the 18-carbon omega-3, alpha-linolenic acid. These findings suggest that higher circulating levels of marine n-3 PUFA are associated with a lower risk of premature death.


The n-3 polyunsaturated fatty acid (PUFA) family has been the subject of intense investigation ever since their inverse associations with risk for acute myocardial infarction were reported in Greenland Eskimos in the 1970s1,2. The PUFAs in this family include the 18-carbon, plant-derived alpha-linolenic acid (ALA,) as well as the 20–22-carbon, long-chain (LC, mostly seafood-derived) eicosapentaenoic (EPA), docosapentaenoic (DPA), and docosahexaenoic (DHA) acids.

The efficacy of the LC n-3 PUFAs in reducing risk for cardiovascular disease (CVD) remains controversial as findings from different randomized controlled trials (RCTs) have been conflicting. Nevertheless, a 2019 meta-analysis of RCTs reported significant reductions in risk for myocardial infarction, coronary heart disease (CHD) events and mortality, and CVD mortality in patients randomized to supplemental LC n-3 PUFAs3. Another meta-analysis of observational studies found that higher levels of circulating LC n-3 PUFA levels were significantly associated with a lower risk for CHD death4. However, no meta-analysis has yet examined the relationship between LC n-3 PUFAs blood levels and risk for all-cause mortality. Indeed, the only meta-analyses to report a beneficial association with all-cause mortality were based on the self-reported intake of fish5,6. Fish contain many nutrients besides just LC n-3 PUFAs, self-reported food intake is memory dependent, food databases can be out of date, and fish meals often replace less healthful choices. As a result, studies that link LC n-3 PUFAs and health outcomes based on self-reported fish intake have potential limitations. A more reliable and objective measure of LC n-3 PUFA consumption is their level in the blood7 which is primarily determined by the consumption of preformed LC n-3 PUFAs (although synthesis from dietary ALA can make a small contribution8). Hence a clearer picture of the biological relationship between LC n-3 PUFAs and disease outcomes may be obtained from biomarker-based investigations.

Some studies have reported inverse relations between n-3 PUFA biomarkers and total mortality9,10,11, while others have not12,13. In the Cardiovascular Health Study, higher LC n-3 PUFA levels also were associated with overall “healthier aging” (i.e., surviving past age 65 free of chronic diseases and maintaining good functional status)14. However, reports from studies of individual cohorts can be limited by insufficient power and inconsistent adjustment for potential confounding factors. In addition, publication bias can distort summary conclusions. To address these challenges, the present study pooled de novo individual-level analyses across 17 prospective cohort studies in the Fatty Acid and Outcome Research Consortium (FORCE)15 to explore the associations of circulating levels of n-3 PUFAs (both plant- and seafood-derived) and all-cause mortality. Secondarily, we examined the associations with mortality from CVD, cancer, and all other causes.

Here, we show significant inverse associations for all mortality endpoints with the LC n-3 PUFA levels. Hence, chronically higher tissue levels of these FAs operating through a variety of potential mechanisms may slow the aging process.



The pooled analyses included circulating n-3 PUFA measurements on 42,466 individuals, 15,720 (37%) of whom died during follow-up (Table 1). At baseline, the average age was 65 years (range of mean ages across cohorts was 50–81 years), 55% were women (range of 0–100% across cohorts) and the median follow-up time was 16 years (range of 5–32 years across cohorts). Whites constituted 87% of the sample. Circulating levels of the n-3 PUFAs (and of the n-6 PUFAs linoleic and arachidonic acids, which were included as covariates) are shown in Supplementary Fig. 1 and in Supplementary Table 2. Supplementary Table 3 shows the number of cause-specific deaths from participating cohorts. Overall, approximately 30% of the deaths were attributed to CVD, 30% to cancer, and the remaining 39% to all other causes.

Full size table

Total mortality

Comparing the medians of the first and fifth quintiles (i.e., approximately the 90th and the 10th percentiles), higher EPA, DPA, DHA, and EPA + DHA levels were associated with between 9% and 13% lower risk of all-cause mortality (Table 2). (The fatty acid levels associated with these percentiles for each cohort and sample type are shown in Supplementary Table 4). The HR for total mortality for EPA + DHA was 0.87 (95% CI: 0.83–0.90) (Fig. 1). In contrast, ALA was not significantly associated with all-cause mortality [HR 0.99 (0.96–1.02)]. In an across quintiles analysis, significant trends were observed for EPA, DPA, DHA, and EPA + DHA (all < 0.01); and comparing the top to the bottom quintile, each was associated with 15–18% lower risk of death (Table 3). There was little evidence for nonlinearity in these inverse associations for all each LC n-3 PUFAs except for EPA (p = 0.002 for the nonlinearity; Fig. 2). The relationship of EPA with mortality was most pronounced at lower levels and then appeared to plateau at higher levels. ALA was generally unassociated with total mortality, except for a borderline association in the top quintile [HR 0.94 (0.89–0.99); P-trend = 0.13], and there was no evidence for nonlinearity (Supplementary Fig. 2).

Full size table

Study-specific estimates for HRs (dark squares) are shown per interquartile range (comparing the midpoint of the top to the bottom quintiles) their sizes indicate study weights (column 3). The horizontal line through each HR is 95% CI. Compartments included erythrocyte phospholipids, plasma phospholipids, cholesteryl esters, and total plasma. All HRs are adjusted for age, sex, race, field center, body-mass index, education, occupation, marital status, smoking, physical activity, alcohol intake, prevalent diabetes, hypertension, and dyslipidemia, self-reported general health, and the sum of circulating n-6 PUFA (linoleic plus arachidonic acids). See Table 1 footnote for abbreviations of cohorts.

Full size image

Full size table

The best estimates and their confidence intervals are presented as black lines and gray-shaded areas, respectively. The 10th percentile was selected as a reference level and the x-axis depicts 5th to 95th percentiles. Potential nonlinearity was identified for EPA (p = 0.0004) but not for the others (p > 0.05). All HRs are adjusted for age, sex, race, field center, body-mass index, education, occupation, marital status, smoking, physical activity, alcohol intake, prevalent diabetes, hypertension, and dyslipidemia, self-reported general health, and the sum of circulating n-6 PUFA (linoleic plus arachidonic acids).

Full size image

Cause-specific mortality

Comparing the 90th to the 10th percentile, each of the LCn-3 PUFAs was significantly associated with a lower risk for death from CVD, cancer, and all other causes combined [except for DHA and cancer mortality, HR 0.93 (0.86–1.00)] (Table 2). ALA was not significantly associated with any cause-specific mortality. Evaluating the trend across quintiles, EPA, DHA, and EPA + DHA were inversely associated with CVD death, EPA and DPA were inversely associated with cancer death, and each of the LC n-3 PUFAs was inversely associated with other death. Comparing the top to the bottom quintile, EPA, DPA, DHA, and EPA + DHA were each significantly, inversely associated with CVD, cancer, and other mortality (Table 3).

Heterogeneity and sensitivity analyses

Inter-cohort heterogeneity was at least moderate (I2 > 50%) in the pooled analyses of all-cause mortality for all n-3 PUFAs except ALA (I2 = 26%) and EPA (I2 = 41%), while heterogeneity for cause-specific mortality ranged from little to moderate (0–56%) (Supplementary Table 5). There was little evidence of differential associations with mortality by PUFA lipid compartment after accounting for multiple testing (5 PUFAs × 4 outcomes; Bonferroni correction 0.05/20 = 0.0025, Supplementary Table 6). Likewise, associations of n-3 PUFAs with total mortality were similar across strata based on age, sex, race, and fish oil use (Supplementary Table 7), with no significant differences after accounting for multiple testing (5 PUFAs × 4 strata results; Bonferroni correction 0.05/20 = 0.0025). Overall findings did not change with the removal of participants taking fish oil (Supplementary Table 7) or in the drop-one-cohort analyses.


In this meta-analysis utilizing a harmonized analytical strategy with individual-level data from 17 cohorts, we examined the associations between circulating levels of the n-3 PUFAs and mortality. We found that, after controlling for other major risk factors, LC n-3 PUFAs (but not ALA) were associated with about a 15–18% lower risk of total mortality comparing the top to the bottom quintiles. These relationships were generally linear for DPA, DHA, and EPA + DHA, but not for EPA. For this PUFA there was a steeper risk reduction across the lower blood levels but little additional difference in risk at higher blood levels. Inverse correlations were also generally observed between LC n-3 PUFA levels and CVD, cancer, and other causes of death.

This pooled analysis including over 40,000 participants and over 15,000 deaths greatly expands upon the findings of prior individual cohort studies that examined associations of circulating levels of n-3 PUFAs and all-cause mortality9,10,11,12,13,16,17,18,19,20,21,22,23,24. Relatively few studies have evaluated self-reported dietary fish (or estimated n-3 PUFA) intake in relation to total mortality, but those that have typically support our observations here5,22,25,26. Interestingly, reported use of fish oil supplements was linked to a lower risk for death from any cause in a study from the UK including over 427,000 individuals27.

Associations with total and cause-specific mortality were not significant for the plant-derived n-3 PUFA ALA. Prior biomarker-based meta-analyses reported inverse associations of ALA with CHD death, but relationships with total or CVD mortality were not examined4,28. Whether our finding of no association ALA on CVD mortality was because ALA has no role to play in fatal strokes (included in the CVD mortality metric) or because of differences in the cohorts included in these prior meta-analyses vs. the present one is not clear. Circulating ALA levels are less dependable markers of intake compared with the LC n-3 PUFAs because this fatty acid is rapidly β-oxidized and, to a small extent, converted into the LC n-3 PUFAs8. Nevertheless, the borderline and inconsistent relations of ALA on mortality risk deserve further study.

Higher circulating levels of LC n-3 PUFAs may beneficially affect diverse cellular systems that together could contribute to a reduced risk for death. The mechanisms behind the ostensibly beneficial effect of LC n-3 PUFAs on human biology are multiple and have been summarized in several recent reviews papers29,30,31,32. Among them are hypotriglyceridemic, antihypertensive, and antiplatelet effects; as well as positive effects on adipocyte biology, endothelial function, and autonomic balance. All of these appear to be mediated by effects on membrane physiochemistry, gene expression, and the production of a myriad of bioactive oxylipins. Persistently lower levels of inflammatory biomarkers also characterize those with higher circulating LC n-3 PUFA levels33. These fatty acids have been reported to inhibit the mammalian (or mechanistic) target of rapamycin (mTOR) in animal studies showing benefits in cancer34, metabolic syndrome35, spinal cord injury36, and depression37. mTOR inhibition extends lifespan in many species38 and acts as an energy sensor to coordinate gene expression, ribosome biogenesis, and mitochondrial metabolism39. In the Heart and Soul Study, where whole blood EPA + DHA levels were inversely associated with all-cause mortality24, higher levels were also linked with a slower rate of telomere shortening over a 5-year period40. As higher rates of telomere attrition have been associated with shorter overall lifespan41,42, this finding may be secondary to the more distal biochemical mechanisms noted above. Regardless of their specific actions, higher cellular levels of the LC n-3 PUFAs appear to slow the aging process.

Our findings of lower risk of CVD death with high vs. low blood levels of EPA + DHA are generally consistent with meta-analyses of self-reported fish intake25 and of biomarker levels4, as well as randomized controlled clinical trials of n-3 PUFA supplementation3,43 (although the most recent trial44 has not yet been included in meta-analyses). Compared with CVD, evidence for a link between n-3 PUFAs and cancer mortality risk is sparse, with no significant relationship for self-reported estimates of fish or n-3 PUFA consumption25,45. Meta-analyses of RCTs with n-3 PUFA supplements also have not observed effects on cancer, although short-term durations of such trials (generally up to 5 years) would likely preclude any ability to detect an effect on cancer46,47. The difference between these findings and what we observed may arise from the use of biomarker levels instead of self-reported fish intake. Biomarkers are potentially truer reflections of long-term exposure, making it easier to detect subtle relationships. In addition, circulating LC n-3 PUFA levels reflect endogenous metabolism, especially for DPA which is not correlated with estimated dietary DPA intake48 but may have important biologic effects49. Finally, since neurodegenerative diseases are a major non-CVD, non-cancer cause of death, a report that higher fish intake was associated with reduced mortality from this cause6 is consistent with our observations here.

Although circulating marine n-3 PUFA levels have not been measured in all of the major intervention trials, the doses of EPA + DHA used in most trials (<1 g/day) may not have resulted in marked differences in levels between treated and control patients50. For example, in the Vitamin D and Omega-3 Trial (VITAL) trial, treatment with 840 mg of EPA + DHA per day increased plasma phospholipid EPA + DHA levels from 2.7 to 4.1%, a 55% increase. This relatively small difference in LC n-3 PUFA levels between the placebo and active treatment groups could be one of the potential reasons for the failure of some RCTs to detect an effect of n-3 PUFAs on CV outcomes50,51. Future RCTs may be more effective if they focus on people with low baseline levels of LC n-3 PUFAs52 and provide doses of EPA and DHA that produce higher blood levels. An intake of about 250 mg of EPA + DHA per day as recommended in the Dietary Guidelines for Americans53 may raise circulating levels into the ranges observed here for some but not all adults7.

Although a significant effect on the primary (composite) endpoint in the VITAL trial47 was not achieved, our findings comport well with some of its secondary findings. In this study, the provision of 840 mg of EPA + DHA/day significantly reduced risk for major CV events and myocardial infarction in those participants with lower (vs. higher) intakes of fish (blood levels in these groups were not reported). There was a significant interaction of fish intake on total mortality as well; the HR (95% CI) in the low intake group was 0.87 (0.73–1.04) and in the high intake group, 1.19 (0.99–1.44, p for interaction 0.017). This secondary observation in VITAL implies that individuals with lower baseline LC n-3 PUFA levels are more likely to benefit from increased levels than those with higher baseline levels. Two recent RCTs examining the effects of high dose (~3–4 g/day) of LC n-3 PUFAs were performed in overweight patients with high blood triglyceride levels and at high risk for CVD events, all on background statin therapy. After 5 years of treatment, Bhatt et al.54 reported beneficial effects of EPA ethyl esters on CV events, whereas Nicholls et al.44 found no effect on the primary outcome using an EPA + DHA product in which the fatty acids were non-esterified. Another 2-year trial in elderly post-MI patients from Norway given 1.8 g of EPA + DHA found no benefit on CV outcomes55. None of these trials is directly relevant to our findings here owing to the nature of the high-risk patient populations, the number of concurrent background medications, the short duration of treatment, and the initiation of treatment late in life.

Strengths of the current analysis include the use of objective n-3 PUFA biomarkers (instead of estimated intakes from dietary questionnaires) which increases the accuracy of exposure assessment and allows for separate analysis of different individual n-3 PUFAs. The use of prespecified, harmonized, de novo individual-level analyses across multiple cohorts substantially increase generalizability, reduces confounding through consistent adjustment for covariates, and limits the potential for publication bias. The pooling of 17 studies including over 15,000 deaths also increased the statistical power to evaluate mortality subtypes as well as potential heterogeneity across subgroups.

Potential limitations deserve attention. Because our outcome was not rare, the hazard ratios (HRs) reported here (instantaneous relative risk) may be modestly different than the cumulative relative risk. Most individuals were White, potentially lowering generalizability to other races/ethnicities, although our analysis still included nearly 6000 non-Whites in whom findings for EPA + DHA were generally similar to those for Whites (Supplementary Table 7). Despite extensive efforts to harmonize study-specific methods, moderate heterogeneity remained between studies that may be due to unmeasured background population characteristics, differences in laboratory assessment of PUFAs and of outcomes, chance, or any combination of these. PUFAs and covariates were measured once at baseline, and changes over time could lead to misclassification, which could bias the results in uncertain directions. On the other hand, reasonable reproducibility has been reported for n-3 PUFA biomarker concentrations over time56. Because analytical methods, even within the same lipid fraction, were not standardized, and n-3 PUFA levels were measured in multiple fractions, we assessed cohort-specific n-3 PUFA percentiles rather than absolute percentages of total fatty acids in each fraction. Since FA levels were reported as a percent of total FAs in each lipid compartment, levels of one FA could affect levels of another. Indeed, in the plasma or RBC PL and CE pools, higher levels of the LC n-3 PUFAs (which were the focus of this study) are linked with lower levels of the n-6 PUFAs but not of saturated or mono-unsaturated FAs57,58. Since we adjusted for differences in linoleic and arachidonic levels in our analyses, this concern was accounted for. Each lipid pool used in this study reflects LC n-3 PUFA intake during relatively different and overlapping time periods generally from months to weeks following this hierarchy: RBC ≥ Plasma PL ≈ Plasma CE ≥ total plasma59,60. In addition, we cannot rule out the potential for residual confounding. That is, higher LC n-3 PUFA levels may simply be markers of a “healthy lifestyle,” and the fatty acids themselves may not be playing any physiological role in postponing death but would be biomarkers of a suite of other healthy behaviors (dietary/exercise/non-smoking, etc.), or endogenous metabolic processes, that might, in a multiplicity of ways, manifest in greater longevity. Although we adjusted for many major risk factors (age, income, marital status, smoking, hyperlipidemia, hypertension, etc.), residual confounding by other factors is always possible. However, the magnitude of the observed effect of the meta-analysis of circulating LC n-3 PUFAs and total mortality reported herein is consistent with the known associations with CHD mortality and sudden cardiac death61,62. Finally, as the attribution of cause of death is never as unambiguous as death itself, some uncertainty must attend to the cause-specific analyses reported here. In summary, in a global pooled analysis of prospective studies, LC n-3 PUFA levels were inversely associated with risk for death from all causes and from CVD, cancer, and other causes.


Study design and population: FORCE Consortium

The study was conducted within FORCE15, a consortium of observational studies with fatty acid biomarker data and ascertained chronic disease events4. For the current project, 48 prospective studies in the consortium as of December 2018 were invited to participate. Of these, seven did not have relevant data (e.g., no mortality outcomes or no circulating PUFA levels at baseline), two included only participants with prevalent CVD, 13 indicated a lack of funding/analyst time and 9 did not respond after at least 5 separate invitations to participate over a 9-month period. The study sample comprised data from 17 studies across 10 countries with available data on circulating PUFA levels at baseline and mortality during follow-up. The details of each individual study are presented in Supplementary Table 1. All participating studies followed a prespecified standardized analysis protocol with harmonized inclusions and exclusions, exposures, outcomes, covariates, and analytical methods including assessment of missing covariate data and statistical models. In each study, new analyses of individual data were performed according to the protocol, and study-specific results were collected using a standardized electronic form. Information regarding registration for any of the cohorts included herein (that required it prior to study initiation) is shown in Supplementary Table 1.

Individual cohorts conducted their studies in accordance with the criteria set by the Declaration of Helsinki, and informed consent was obtained from all participants.

Study participants in the included cohorts (a) were >18 years old, (b) had no major medical diagnoses (prior myocardial infarction, prior stroke, severe active cancer, severe renal disease, severe liver, or lung disease), (c) were not taking supplemental fish oil, and (d) did not die within a year of baseline. The one exception to (c) was the inclusion of the Age, Genes, Environment Susceptibility Study (Reykjavik) (AGES-R) from Iceland63 in which 68% of participants reported taking cod liver oil. This factor was adjusted for in the AGES-R analysis, and participants in AGES-R taking cod liver oil were also excluded in a sensitivity analysis.

Fatty acid measurements

Participating studies measured PUFAs in at least one blood compartment, including plasma phospholipids, cholesterol esters, erythrocytes, and whole plasma. All PUFA levels were reported as a percent of total fatty acids. Detailed information regarding PUFA measurement methods for each study is in Supplementary Table 1.

Outcome assessment

The primary endpoint of this study was total mortality (death from any cause). Additional endpoints of interest were deaths from CVD, cancer, and all other causes. Detailed information on the definitions of the outcomes used in each cohort is included in Supplementary Table 1.


Prespecified covariates included age (continuous), sex (men/women), race (binary: White/non-White), field center (categories), body-mass index (continuous), education (less than high school graduate, high school graduate, at least some college or vocational school), occupation (if available), marital status (married, never married, widowed, divorced), smoking (current, former, never), physical activity (kcal/week, METS/week, or hours/day), alcohol intake (drinks or servings/day, g/day or ml/day), prevalent diabetes mellitus (treated or physician-diagnosed), prevalent hypertension (treated or physician-diagnosed), prevalent dyslipidemia (treated or physician-diagnosed), self-reported general health (if available) and circulating n-6 PUFA levels (i.e., the sum of linoleic and arachidonic acids). If individual cohorts could not categorize these covariates exactly according to these definitions, then study-specific categories were used as surrogates. Missing variables were handled as detailed in the Online Supplementary Materials.

Statistical analysis and pooling

Study-specific analyses were harmonized across cohorts. They were carried out using Cox proportional hazards models using robust variance estimates to calculate the multivariable-adjusted HRs in each study, with follow-up from the date of biomarker measurement to date of death, loss to follow-up, or end of follow-up. Associations and relevant statistical interactions were also assessed in prespecified strata within each cohort by age (<60 vs. ≥60), sex, and race (White vs. non-White). To allow comparison and pooling of results from different biomarker compartments, n-3 PUFA levels were standardized to the study-specific inter-quintiles range defined as the range between the medians of the top and bottom quintile categories (i.e., about the 90th and 10th percentiles). In addition, each cohort computed HRs across study-specific quintiles, with the lowest quintile as the reference. Pooling by quintiles instead of absolute fatty acid values were necessary because values differ by lipid compartment. Nevertheless, such an approach was reasonable given the observed correlations among different lipid compartments. For example, the Pearson correlations between EPA + DHA levels (i.e., percent of total fatty acids) in RBC and CE, PL, and whole plasma are 0.83, 0.88, and 0.93, respectively (unpublished data from Harris lab based on 49 samples analyzed in all four compartments).


Cohort-specific HRs were pooled by inverse-variance weighted meta-analysis. Heterogeneity was assessed by the I2 statistic and Q-test. Heterogeneity was further explored by meta-analyzing prespecified subgroups. Sensitivity analyses included (1) the removal of those subjects from AGES-R who reported fish oil use, and (2) re-analysis after the removal of each cohort one at a time. The potential for a nonlinear association of each n-3 PUFA with all-cause mortality was examined with a multivariable meta-analysis with a restricted cubic spline technique64 as detailed in Online Supplementary Materials. Stata 15.1 (Stata Corp., College Station, TX) was used for spline fitting and testing. All the other meta-analyses were conducted using the metafor package65 in R version 366. A two-tailedP value of <0.05 was considered to be statistically significant unless otherwise specified, e.g., in the exploratory analyses by subgroups and lipid compartments.

Reporting summary

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

Data availability

Policies for data-sharing vary between the cohorts depending on their original human subjects' approvals and existing procedures. For approved data-sharing requests, types of data that may be shared can include demographics, exposures, covariates, and outcomes. Please contact each individual principal investigator for cohort-specific data requests (See Supplementary Table 1).


  1. 1.

    Dyerberg, J., Bang, H. O., Stoffersen, E., Moncada, S. & Vane, J. R. Eicosapentaenoic acid and prevention of thrombosis and atherosclerosis? Lancet2, 117–119 (1978).

  2. 2.

    Bang, H. O. & Dyerberg, J. Lipid metabolism and ischemic heart disease in greenland eskimos. Adv. Nutr. Res.3, 1–22 (1980).

    CAS Google Scholar

  3. 3.

    Hu, Y., Hu, F. B. & Manson, J. E. Marine omega-3 supplementation and cardiovascular disease: an updated meta-analysis of 13 randomized controlled trials involving 127 477 participants. J. Am. Heart Assoc.8, e013543 (2019).

    PubMedPubMed Central Google Scholar

  4. 4.

    Del Gobbo, L. C. et al. Omega-3 polyunsaturated fatty acid biomarkers and coronary heart disease: pooling project of 19 cohort studies. JAMA Intern. Med.176, 1155–1166 (2016).

    PubMedPubMed Central Google Scholar

  5. 5.

    Wan, Y., Zheng, J., Wang, F. & Li, D. Fish, long chain omega-3 polyunsaturated fatty acids consumption, and risk of all-cause mortality: a systematic review and dose-response meta-analysis from 23 independent prospective cohort studies. Asia Pac. J. Clin. Nutr.26, 939–956 (2017).

    CASPubMed Google Scholar

  6. 6.

    Wang, D. D. et al. Association of specific dietary fats with total and cause-specific mortality. JAMA Intern. Med.176, 1134–1145 (2016).

    PubMedPubMed Central Google Scholar

  7. 7.

    Jackson, K. H., Polreis, J. M., Tintle, N. L., Kris-Etherton, P. M. & Harris, W. S. Association of reported fish intake and supplementation status with the omega-3 index. Prostaglandins Leukotrienes Essent. Fat. Aacids142, 4–10 (2019).

    CAS Google Scholar

  8. 8.

    Barcelo-Coblijn, G. & Murphy, E. J. Alpha-linolenic acid and its conversion to longer chain n-3 fatty acids: benefits for human health and a role in maintaining tissue n-3 fatty acid levels. Prog. Lipid Res.48, 355–374 (2009).

    CASPubMed Google Scholar

  9. 9.

    Harris, W. S. et al. Red blood cell polyunsaturated fatty acids and mortality in the Women’s Health Initiative Memory Study. J. Clin. Lipidol.11, 250–259 (2017).

    PubMedPubMed Central Google Scholar

  10. 10.

    Harris, W. S., Tintle, N. L., Etherton, M. R. & Vasan, R. S. Erythrocyte long-chain omega-3 fatty acid levels are inversely associated with mortality and with incident cardiovascular disease: the Framingham Heart Study. J. Clin. Lipidol.12, 718–724 (2018).

    PubMedPubMed Central Google Scholar

  11. 11.

    Mozaffarian, D. et al. Plasma phospholipid long-chain omega-3 fatty acids and total and cause-specific mortality in older adults: a cohort study. Ann. Intern. Med.158, 515–525 (2013).

    PubMedPubMed Central Google Scholar

  12. 12.

    Iggman, D., Arnlov, J., Cederholm, T. & Riserus, U. Association of adipose tissue fatty acids with cardiovascular and all-cause mortality in elderly men. JAMA Cardiol.1, 745–753 (2016).

    PubMed Google Scholar

  13. 13.

    Chien, K. L. et al. Comparison of predictive performance of various fatty acids for the risk of cardiovascular disease events and all-cause deaths in a community-based cohort. Atherosclerosis230, 140–147 (2013).

    CASPubMed Google Scholar

  14. 14.

    Lai, H. T. et al. Serial circulating omega 3 polyunsaturated fatty acids and healthy ageing among older adults in the Cardiovascular Health Study: prospective cohort study. Br. Med. J.363, k4067 (2018).

    Google Scholar

  15. 15.

    FORCE. Fatty Acids and Outcomes Research Consortium. (2020).

  16. 16.

    Miura, K., Hughes, M. C. B., Ungerer, J. P. & Green, A. C. Plasma eicosapentaenoic acid is negatively associated with all-cause mortality among men and women in a population-based prospective study. Nutr. Res.36, 1202–1209 (2016).

    CASPubMed Google Scholar

  17. 17.

    Lindberg, M., Saltvedt, I., Sletvold, O. & Bjerve, K. S. Long-chain n-3 fatty acids and mortality in elderly patients. Am. J. Clin. Nutr.88, 722–729 (2008).

    CASPubMed Google Scholar

  18. 18.

    Kleber, M. E., Delgado, G. E., Lorkowski, S., Marz, W. & von Schacky, C. Omega-3 fatty acids and mortality in patients referred for coronary angiography. The Ludwigshafen Risk and Cardiovascular Health Study. Atherosclerosis252, 175–181 (2016).

    CASPubMed Google Scholar

  19. 19.

    Chen, G. C., Yang, J., Eggersdorfer, M., Zhang, W. & Qin, L. Q. N-3 long-chain polyunsaturated fatty acids and risk of all-cause mortality among general populations: a meta-analysis. Sci. Rep.6, 28165 (2016).

    ADSCASPubMedPubMed Central Google Scholar

  20. 20.

    Matsuda, H. et al. Evaluation of a high serum docosahexaenoic acid level as a predictor of longevity among elderly residents at a special nursing home. Geriatr. Gerontol. Int.18, 980–982 (2018).

    PubMed Google Scholar

  21. 21.

    Wang, Y. et al. Fish consumption, blood docosahexaenoic acid and chronic diseases in Chinese rural populations. Comp. Biochem. Physiol. A Mol. Integr. Physiol.136, 127–140 (2003).

    PubMed Google Scholar

  22. 22.

    Otsuka, R. et al. Fish and meat intake, serum eicosapentaenoic acid and docosahexaenoic acid levels, and mortality in community-dwelling Japanese Older Persons. Int. J. Environ. Res. Public Health16, 1806 (2019).

    CASPubMed Central Google Scholar

  23. 23.

    Virtanen, J. K. et al. Mercury, fish oils, and risk of acute coronary events and cardiovascular disease, coronary heart disease, and all-cause mortality in men in eastern Finland. Arterioscler. Thromb. Vasc. Biol.25, 228–233 (2005).

    CASPubMed Google Scholar

  24. 24.

    Pottala, J. V., Garg, S., Cohen, B. E., Whooley, M. A. & Harris, W. S. Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul Study. Circ. Cardiovasc. Qual. Outcomes3, 406–412 (2010).

    PubMedPubMed Central Google Scholar

  25. 25.

    Zhang, Y. et al. Association of fish and long-chain omega-3 fatty acids intakes with total and cause-specific mortality: prospective analysis of 421 309 individuals. J. Intern. Med.284, 399–417 (2018).

    CASPubMed Google Scholar

  26. 26.

    Bell, G. A. et al. Intake of long-chain omega-3 fatty acids from diet and supplements in relation to mortality. Am. J. Epidemiol.179, 710–720 (2014).

    PubMedPubMed Central Google Scholar

  27. 27.

    Li, Z.-H. et al. Associations of habitual fish oil supplementation with cardiovascular outcomes and all cause mortality: evidence from a large population based cohort study. Br. Med. J.368, m456 (2020).

    Google Scholar

  28. 28.

    Pan, A. et al. α-Linolenic acid and risk of cardiovascular disease: a systematic review and meta-analysis. Am. J. Clin. Nutr.96, 1262–1273 (2012).

    CASPubMedPubMed Central Google Scholar

  29. 29.

    Darwesh, A. M., Sosnowski, D. K., Lee, T. Y., Keshavarz-Bahaghighat, H. & Seubert, J. M. Insights into the cardioprotective properties of n-3 PUFAs against ischemic heart disease via modulation of the innate immune system. Chemistry308, 20–44 (2019).

    CAS Google Scholar

  30. 30.

    Wu, J. H. Y., Micha, R. & Mozaffarian, D. Dietary fats and cardiometabolic disease: mechanisms and effects on risk factors and outcomes. Nat. Rev. Cardiol.16, 581–601 (2019).

    PubMed Google Scholar

  31. 31.

    Endo, J. & Arita, M. Cardioprotective mechanism of omega-3 polyunsaturated fatty acids. J. Cardiol.67, 22–27 (2016).

    PubMed Google Scholar

  32. 32.

    Serhan, C. N., Dalli, J., Colas, R. A., Winkler, J. W. & Chiang, N. Protectins and maresins: New pro-resolving families of mediators in acute inflammation and resolution bioactive metabolome. Biochim. Biophys. Acta1851, 397–413 (2015).

    CASPubMed Google Scholar

  33. 33.

    Farzaneh-Far, R., Harris, W. S., Garg, S., Na, B. & Whooley, M. A. Inverse association of erythrocyte n-3 fatty acid levels with inflammatory biomarkers in patients with stable coronary artery disease: the Heart and Soul Study. Atherosclerosis205, 538–543 (2009).

    CASPubMed Google Scholar

  34. 34.

    Chen, Z. et al. mTORC1/2 targeted by n-3 polyunsaturated fatty acids in the prevention of mammary tumorigenesis and tumor progression. Oncogene33, 4548–4557 (2014).

    CASPubMed Google Scholar

  35. 35.

    Liu, R. et al. High ratio of ω-3/ω-6 polyunsaturated fatty acids targets mTORC1 to prevent high-fat diet-induced metabolic syndrome and mitochondrial dysfunction in mice. J. Nutr. Biochem.79, 108330 (2020).

    CASPubMed Google Scholar

  36. 36.

    Nie, J. et al. Inhibition of mammalian target of rapamycin complex 1 signaling by n-3 polyunsaturated fatty acids promotes locomotor recovery after spinal cord injury. Mol. Med. Rep.17, 5894–5902 (2018).

    CASPubMedPubMed Central Google Scholar

  37. 37.

    Deyama, S. et al. Resolvin D1 and D2 reverse lipopolysaccharide-induced depression-like behaviors through the mTORC1 signaling pathway. Int. J. Neuropsychopharmacol.20, 575–584 (2017).

    CASPubMedPubMed Central Google Scholar

  38. 38.

    Papadopoli, D. et al. mTOR as a central regulator of lifespan and aging. F1000Res8, 998 (2019).

    CAS Google Scholar

  39. 39.

    Bjedov, I. & Rallis, C. The target of rapamycin signalling pathway in ageing and lifespan regulation. Genes11, 1043 (2020).

    CASPubMed Central Google Scholar

  40. 40.

    Farzaneh-Far, R. et al. Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. J. Am. Med. Assoc.303, 250–257 (2010).

    CAS Google Scholar

  41. 41.

    Bernadotte, A., Mikhelson, V. M. & Spivak, I. M. Markers of cellular senescence. Telomere shortening as a marker of cellular senescence. Aging8, 3–11 (2016).

    CASPubMedPubMed Central Google Scholar

  42. 42.

    Arbeev, K. G. et al. Association of leukocyte telomere length with mortality among adult participants in 3 longitudinal studies. JAMA Netw. Open3, e200023 (2020).

    PubMedPubMed Central Google Scholar

  43. 43.

    Bernasconi, A. A., Wiest, M. M., Lavie, C. J., Milani, R. V. & Laukkanen, J. A. Effect of omega-3 dosage on cardiovascular outcomes: an updated meta-analysis and meta-regression of Interventional Trials. Mayo Clin. Proc.96, 304–313 (2021).

    CASPubMed Google Scholar

  44. 44.

    Nicholls, S. J. et al. Effect of high-dose omega-3 fatty acids vs corn oil on major adverse cardiovascular events in patients at high cardiovascular risk: the STRENGTH Randomized Clinical Trial. J. Am. Med. Assoc.324, 2268–2280 (2020).

    CAS Google Scholar

  45. 45.

    Zhang, Z. et al. Poultry and fish consumption in relation to total cancer mortality: a meta-analysis of prospective studies. Nutr. Cancer70, 204–212 (2018).

    CASPubMed Google Scholar

  46. 46.

    Zhang, Y. F., Gao, H. F., Hou, A. J. & Zhou, Y. H. Effect of omega-3 fatty acid supplementation on cancer incidence, non-vascular death, and total mortality: a meta-analysis of randomized controlled trials. BMC Public Health14, 204 (2014).

    CASPubMedPubMed Central Google Scholar

  47. 47.

    Manson, J. E. et al. Marine n-3 fatty acids and prevention of cardiovascular disease and cancer. N. Engl. J. Med.380, 23–32 (2019).

    CASPubMed Google Scholar

  48. 48.

    Richter, C. K. et al. n-3 Docosapentaenoic acid intake and relationship with plasma long-chain n-3 fatty acid concentrations in the United States: NHANES 2003-2014. Lipids54, 221–230 (2019).

    CASPubMedPubMed Central Google Scholar

  49. 49.

    Drouin, G., Rioux, V. & Legrand, P. The n-3 docosapentaenoic acid (DPA): a new player in the n-3 long chain polyunsaturated fatty acid family. Biochimie159, 36–48 (2019).

    CASPubMed Google Scholar

  50. 50.

    Meyer, B. J. & Groot, R. H. M. Effects of omega-3 long chain polyunsaturated fatty acid supplementation on cardiovascular mortality: the importance of the dose of DHA. Nutrients9, 1305 (2017).

    PubMed Central Google Scholar

  51. 51.

    von Schacky, C. Meta-analysing randomised controlled trials with omega-3 fatty acids in cardiovascular disease. Evid. Based Med.18, e33 (2013).

    Google Scholar

  52. 52.

    Rice, H. B. et al. Conducting omega-3 clinical trials with cardiovascular outcomes: proceedings of a workshop held at ISSFAL 2014. Prostaglandins Leukotrienes Essent. Fat. Acids107, 30–42 (2016).

    CAS Google Scholar

  53. 53.

    U.S. Department of Agriculture, A.R.S. Dietary Guidelines for Americans 2015–2020. (2015).

  54. 54.

    Bhatt, D. L. et al. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N. Engl. J. Med.380, 11–22 (2019).

    CASPubMed Google Scholar

  55. 55.

    Kalstad, A. A. et al. Effects of n-3 fatty acid supplements in elderly patients after myocardial infarction: a randomized controlled trial. Circulation143, 528–539 (2021).

    PubMed Google Scholar

  56. 56.

    Harris, W. S., Pottala, J. V., Vasan, R. S., Larson, M. G. & Robins, S. J. Changes in erythrocyte membrane trans and marine fatty acids between 1999 and 2006 in older Americans. J. Nutr.142, 1297–1303 (2012).

    CASPubMedPubMed Central Google Scholar

  57. 57.

    Flock, M. R. et al. Determinants of erythrocyte omega-3 fatty acid content in response to fish oil supplementation: a dose-response randomized controlled trial. J. Am. Heart Assoc.2, e000513 (2013).

    PubMedPubMed Central Google Scholar

  58. 58.

    Young, A. J. et al. Blood fatty acid changes in healthy young Americans in response to a 10-week diet that increased n-3 and reduced n-6 fatty acid consumption: a randomised controlled trial. Br. J. Nutr.117, 1257–1269 (2017).

  59. 59.

    Arab, L. Biomarkers of fat and fatty acid intake. J. Nutr.133, 925S–932S (2003).

    CASPubMed Google Scholar

  60. 60.

    Hodson, L., Skeaff, C. M. & Fielding, B. A. Fatty acid composition of adipose tissue and blood in humans and its use as a biomarker of dietary intake. Prog. Lipid Res.47, 348–380 (2008).

    CASPubMed Google Scholar

  61. 61.

    Siscovick, D. S. et al. Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest. J. Am. Med. Assoc.274, 1363–1367 (1995).

    CAS Google Scholar

  62. 62.

    Albert, C. M. et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N. Engl. J. Med.346, 1113–1118 (2002).

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How to Safely Clean and Disinfect for Coronavirus

How to Safely Clean and Disinfect for Coronavirus

6/24/2020 | Nina Hwang, MPH

Are you concerned about properly disinfecting for coronavirus while also protecting people from the health risks associated with hazardous chemical exposure? 

Green Seal’s new Guidelines for Safer COVID-19 Cleaning and Disinfection spell out five effective and responsible cleaning practices for occupant health and safety during the pandemic. 

Improper cleaning and disinfection practices – such as neglecting required product contact times, using inappropriate procedures or application methods, or failing to communicate with cleaning workers and building tenants – can expose building occupants to unsafe levels of hazardous chemicals while failing to protect them from COVID-19.

Our Guidelines explain how to:

 Earn LEED Credit 

Implementing the five best practices can contribute to earning the new LEED® Pilot Credit - Safety First: Cleaning and Disinfecting Your Space, promoting easy adoption by project managers seeking LEED® credit. The Guidelines also align with the requirements in the features related to cleaning products, practices, and protocols in WELL v2 and the recently announced WELL Health Safety Rating for Facilities Management and Operations. 

Green Seal-certified cleaning services already are verified to meet strict third-party standards for safe and effective cleaning and disinfecting, including rigorous requirements for training and operations. The Guidelines provide these best-in-class cleaning services additional guidance for pandemic-specific practices.

Safer Disinfecting Ingredients for COVID-19

When it comes to disinfectants that are effective against the virus that causes COVID-19, some active ingredients are safer than others. While EPA does not allow third-party certifications for disinfectants, Green Seal has curated U.S. EPA’s List N: Disinfectants for Coronavirus to help you identify safer ones.

Green Seal recommends choosing List N disinfectants with the following active ingredients. Unlike other active ingredients commonly found in disinfectants, the active ingredients we recommend are not linked to asthma, cancer, endocrine disruption, DNA damage or skin irritation. 

  • hydrogen peroxide**
  • citric acid
  • lactic acid
  • ethyl alcohol (also called ethanol or just alcohol)
  • isopropyl alcohol
  • peroxyacetic acid** 
  • hypochlorous acid

Products With Safer Disinfecting Ingredients

Green Seal has compiled a list of EPA List N disinfectants that use safer active ingredients. This is only a partial list; check List N for other options. As always, read the label carefully and follow the directions for safe, effective use.

  • Accel 5 RTU
    EPA Registration No. 74559-8 • 5-minute contact time
  • Angel
    EPA Registration No. 777-126 • 10-minute contact time
  • Annihilyte 
    EPA Registration No. 92449-1 • 10-minute contact time
  • Bona STL Disinfecting Cleaner
    EPA Registration No. 91861-2 • 10-minute contact time
  • CleanCide
    EPA Registration No. 34810-35 • 5-minute contact time
  • Diversey’s Oxivir TB Ready-to-Use Liquid
    EPA Registration No. 70627-56 • 1-minute contact time
  • Ecolab’s Peroxide Multi Surface Cleaner and Disinfectant
    EPA Registration No. 1677-238 • 2-minute contact time
  • ECOS Multi-Purpose Disinfectant & Sanitizer, fresh citrus
    EPA Registration No.34810-35-82206•5-minute contacttime
  • ECOS Multi-Purpose Disinfectant Wipes, fresh citrus
    EPA Registration No. 34810-37-82206 • 3-minute contact time
  • ECOS PRO Multi-Surface Disinfectant & Sanitizer, fresh citrus
    EPA Registration No. 34810-35-82206 • 5-minute contact time
  • Facility + RTU
    EPA Registration No. 45745-12 • 1-minute contact time
  • Force of Nature Activator Capsule***
    EPA Registration No. 93040-1 • 10-minute contact time
  • Hydra
    EPA Registration No. 10772-21 • 5-minute contact time
  • Lemi Shine Disinfecting Wipes 
    EPA Registration No. 34810-37-92388 • 3-minute contact time
  • PURELL Healthcare Surface Disinfectant 
    EPA Registration No. 84368-1-84150 • 30-second contact time
  • PURELL Professional Food Service Surface Sanitizer 
    EPA Registration No. 84368-1-84150 • 30-second contact time
  • PURELL Professional Surface Disinfectant 
    EPA Registration No. 84368-1-84150 • 30-second contact time
  • UrthPRO
    EPA Registration No. 84368-1 • 30-second contact time
  • Viking Pure Disinfectant
    EPA Registration No. 87542-1 • 10-minute contact time
  • Wexford Disinfectant Wipes EPA Registration
    No. 34810-37 • 3-minute contact time
  • Windex Disinfectant Cleaner 
    EPA Registration No. 4822-593 • 10-minute contact time

It is also important to look at the safety of the overall disinfectant product, including inactive ingredients. The product safety data sheet (SDS) provides information on whether the overall product is classified as hazardous according to the Occupational Safety and Health Administration.

**The combination of hydrogen peroxide and peroxyacetic acid is a designated AOEC asthmagen, so avoid products that contain both.
***Force of Nature is a Green Seal-certified device generated solution 

How to Make Force of Nature Electrolyzed Water Multi-Purpose Cleaner \u0026 Natural Disinfectant At Home

Exhibitor Press Releases

CANTON, MA, January 1 2020: HT Berry Co., Inc, Massachusetts premier distributor of paper and janitorial products has today announced an exciting new partnership with Force of Nature company. The agreement involves the distribution of Force of Nature, a new and highly innovative, electrolyzed water cleaner and EPA Certified disinfectant. Bringing the proven technology of activated electrolyzed water as a cleaner and disinfectant from the realm of industrial manufacturing to schools, daycares and business throughout New England.

Force of Nature is an appliance that turns tap water, plus a capsule of salt, water, and vinegar into a cleaner, deodorizer and disinfectant as effective as bleach. It is a multi-purpose cleaner that kills 99.9% of germs with no toxic chemicals. It powers through grease, grime, sticky messes, soap scum, odors, and germs as effectively as bleach with no toxic fumes or residues. It cleans virtually any surface – sealed stone, glass, stainless steel, wood, laminate, porcelain, composite, grout, tile, plastic & rubber.

Force of Nature is a patent-pending appliance that uses electricity to change the chemical composition of salt, water and vinegar into a powerful cleaner & disinfectant from the industrial space called electrolyzed water. Electrolyzed water has no harmful ingredients, residues or fumes and contains just 2 gentle, yet potent ingredients:
• Hypochlorous acid – a disinfectant that’s as effective as bleach. Hypochlorous acid is the same substance your white blood cells produce to fight infection, and it’s commonly the active ingredient in wound, eye and veterinary care products because it’s so gentle and effective. Hypochlorous acid is gentle enough to spray on the surfaces children come into contact with.
• Sodium hydroxide – a detergent & grease-cutter without suds. Contains just 0.0000003% yet cleans as well as major brands that have up to 5%.

Force of Nature is an EPA registered disinfectant & sanitizer that kills 99.9% of germs*, including Salmonella, Norovirus, Listeria, STAPH, MRSA, Pseudomonas & Influenza A when used as directed. It exceeds the EPA standard as an anti-microbial disinfectant. The EPA has certified Force of Nature for use in hospitals, schools, daycares, veterinary clinics and more. The registration number is #93040-1. To secure the EPA registration, a product is tested using extremely rigorous EPA approved anti-microbial testing protocols, in EPA approved labs, over multiple lots. Suppliers, purity, concentration & processing of all individual ingredients have to be approved, with strict statistical limits on all. The product also goes through rigorous safety reviews.

Commenting on the agreement, Jane Berry, CEO at HT Berry Co., Inc said " Offering a nontoxic green alternative to traditional cleaning products allows us to provide our customers with an eco-friendly safe multi-purpose cleaner, disinfectant and sanitizer.  This unique product aligns with our Healthy and Sustainable Solutions platforms for providing products that help keep people and the environment healthy by limiting the effects of harsh chemicals.”

For more information on Force of Nature please call 1-781-828-6000 or visit


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