Associations between urine glyphosate levels and metabolic health risks: insights from a large cross-sectional population-based study.

BACKGROUND: The prevalence of metabolic syndrome (MetS) in American adults increased from 37.6% in the 2011-12 period to 41.8% in 2017-2018. Environmental exposure, particularly to common compounds such as glyphosate, has drawn increasing attention as a potential risk factor. METHODS: We employed three cycles of data (2013-2018) from the National Health and Nutrition Examination Survey (NHANES) in a cross-sectional study to examine potential associations between urine glyphosate measurements and MetS incidence. We first created a MetS score using exploratory factor analysis (EFA) of the International Diabetes Federation (IDF) criteria for MetS, with data drawn from the 2013-2018 NHANES cycles, and validated this score independently on an additional associated metric, the albumin-to-creatinine (ACR) ratio. The score was validated via a machine learning approach in predicting the ACR score via binary classification and then used in multivariable regression to test the association between quartile-categorized glyphosate exposure and the MetS score. RESULTS: In adjusted multivariable regressions, regressions between quartile-categorized glyphosate exposure and MetS score showed a significant inverted U-shaped or saturating dose‒response profile, often with the largest effect for exposures in quartile 3. Exploration of potential effect modification by sex, race, and age category revealed significant differences by race and age, with older people (aged > 65 years) and non-Hispanic African American participants showing larger effect sizes for all exposure quartiles. CONCLUSIONS: We found that urinary glyphosate concentration is significantly associated with a statistical score designed to predict MetS status and that dose-response coefficient is nonlinear, with advanced age and non-Hispanic African American, Mexican American and other Hispanic participants exhibiting greater effect sizes.

Effects of mixtures of polychlorinated biphenyls (PCBs) and three organochlorine pesticides on cognitive function differ between older Mohawks at Akwesasne and older adults in NHANES.

BACKGROUND: Akwesasne Mohawks has been exposed to high concentrations of polychlorinated biphenyls (PCBs) and background levels of organochlorine pesticides, hexachlorobenzene (HCB), dichlorodiphenyl dichloroethylene (DDE), and mirex. We have previously reported relative contributions to the mixture of low- and high-chlorinated PCBs, HCB, and DDE on cognitive decrements in Mohawks of various ages. OBJECTIVE: This study examines differences in the mixture effects of PCB congener groups, HCB, DDE, and mirex on cognitive function in older Mohawks and less PCB-exposed older adults from the National Health and Nutrition Examination Survey (NHANES) 1999-2002 cycles. METHODS: We used Bayesian kernel machine regression (BKMR) to evaluate the mixture effects of different PCB congener groups, HCB, DDE, and mirex on cognitive function in both populations. Models were adjusted for age, sex, education levels, and race/ethnicity focusing on individuals 60 years and older. RESULTS: Older Mohawks had 3-fold higher mean total PCB concentrations and 1.8-fold higher mirex, but slightly lower mean DDE and HCB levels than NHANES older adults. Higher mixture concentrations were significantly associated with greater cognitive decline. In older Mohawks, low- and high-chlorinated PCBs, HCB, and DDE contributed to the cognitive score decline. In contrast, score decline in older NHANES adults were primarily from high-chlorinated PCBs and DDE with a threshold dose of approximately 2.08-2.27 ng/g and 2.02-2.40 ng/g, respectively. CONCLUSION: Mixtures of PCBs and organochlorine pesticides increase the risk of cognitive decline in both older Mohawks and NHANES older adults. However, contributions to these mixture effects show significant differences. In older Mohawks, high- and low-chlorinated PCBs, DDE, and HCB are the primary contributors, while high-chlorinated PCBs and DDE are important contributors in NHANES older adults. Due to chronic heavy exposures to PCBs, older Mohawks had a significantly increased risk of cognitive decline compared to general older adults from NHANES.

State of gaseous air pollutants and resulting health effects in Karachi, Pakistan.

Karachi, Pakistan, is a priority site for air pollution research due to high emissions of air pollutants from vehicular traffic, industrial activities, and biomass burning, as well as rapid growth in population. The objectives of this study were to investigate the levels of gaseous pollutants (NO, NO2, O3, HNO3, and SO2) in Karachi, to determine temporal and seasonal variations, to compare Karachi's air quality with other urban centers, to identify relationships with meteorological conditions, to identify source characterization, and to perform a backward-in-time trajectory analysis and a health impact assessment. Daily samples of gaseous pollutants were collected for six consecutive weeks in each of the four seasons for a year. Daily maximum concentrations of NO (90 parts per billion by volume (ppbv)), NO2 (28.1 ppbv), O3 (57.8 ppbv), and SO2 (331 ppbv) were recorded in fall, while HNO3 (9129 parts per trillion by volume (pptv)) was recorded in spring. Seasonal average concentrations were high in winter for NO (9.47 ± 7.82 ppbv), NO2 (4.84 ± 3.35 ppbv), and O3 (8.92 ± 7.65 ppbv), while HNO3 (629 ± 1316 pptv) and SO2 (20.2 ± 39.4 ppbv) were high in spring and fall, respectively. The observed SO2 seasonal average concentration in fall (20.2 ± 39.4) was 5 times higher than that in summer (3.97 ± 2.77) with the fall 24-h average (120 ppbv) exceeding the WHO daily guideline (7.64 ppbv) by a factor of about 15.7. A health impact assessment estimated an increase of 1200 and 569 deaths due to short-term exposure to SO2 in fall and spring, respectively. Chronic daily intake estimated risk per 1000 was 0.99, 0.47, 0.45, and 0.26 for SO2 in fall, NO in winter, O3 in winter, and NO2 in spring, respectively. This study confirms the effect of poor urban air quality on public health and demonstrated the influence of photochemical reactions as well as unfavorable meteorological conditions on the formation of secondary pollutants.

Effects of glyphosate and glyphosate-based herbicides like Roundup™ on the mammalian nervous system: A review.

Glyphosate is the active ingredient in glyphosate-based herbicides (GBHs), such as Roundup™, the most widely used herbicides in the world. Glyphosate targets an essential enzyme in plants that is not found in animals. However, both glyphosate and GBHs are rated as Group 2A, probable human carcinogens, and also have documented effects on reproduction, acting as endocrine disruptive chemicals. We have reviewed reports of the effects of glyphosate and GBHs on mammalian nervous system function. As with several other herbicides, GBHs exposure has been associated with an increased risk of Parkinson's Disease and death of neurons in the substantia nigra. There is also some evidence implicating Roundup™ in elevated risk of autism. Other studies have shown the effects of GBHs on synaptic transmission in animal and cellular studies. The major mechanism of action appears to be oxidative stress, accompanied by mitochondrial dysfunction. In addition, some gut bacteria utilize the enzyme used by plants, and glyphosate and GBHs use has been shown to alter the gut microbiome. There is a large and growing body of evidence that the gut microbiome alters susceptibility to great number of human diseases, including nervous system function. The weight of the evidence indicates that in addition to cancer and reproductive effects, glyphosate and GBHs have significant adverse effects on the brain and behavior and increase the risk of at least some serious neurological diseases.

Health disparities: Intracellular consequences of social determinants of health.

Health disparities exist dependent on socioeconomic status, living conditions, race/ethnicity, diet, and exposures to environmental pollutants. Herein, the various exposures contributing to a person's exposome are collectively considered social determinants of health (SDOH), and the SDOH-exposome impacts health more than health care. This review discusses the extent of evidence of the physiologic consequences of these exposures at the intracellular level. We consider how the SDOH-exposome, which captures how individuals live, work and age, induces cell processes that modulate a conceptual "redox rheostat." Like an electrical resistor, the SDOH-exposome, along with genetic predisposition and age, regulate reductive and oxidative (redox) stress circuits and thereby stimulate inflammation. Regardless of the source of the SDOH-exposome that induces chronic inflammation and immunosenescence, the outcome influences cardiometabolic diseases, cancers, infections, sepsis, neurodegeneration and autoimmune diseases. The endogenous redox rheostat is connected with regulatory molecules such as NAD+/NADH and SIRT1 that drive redox pathways. In addition to these intracellular and mitochondrial processes, we discuss how the SDOH-exposome can influence the balance between metabolism and regulation of immune responsiveness involving the two main molecular drivers of inflammation, the NLRP3 inflammasome and NF-κB induction. Mitochondrial and inflammasome activities play key roles in mediating defenses against pathogens and controlling inflammation before diverse cell death pathways are induced. Specifically, pyroptosis, cell death by inflammation, is intimately associated with common disease outcomes that are influenced by the SDOH-exposome. Redox influences on immunometabolism including protein cysteines and ion fluxes are discussed regarding health outcomes. In summary, this review presents a translational research perspective, with evidence from in vitro and in vivo models as well as clinical and epidemiological studies, to outline the intracellular consequences of the SDOH-exposome that drive health disparities in patients and populations. The relevance of this conceptual and theoretical model considering the SARS-CoV-2 pandemic are highlighted. Finally, the case of asthma is presented as a chronic condition that is modified by adverse SDOH exposures and is manifested through the dysregulation of immune cell redox regulatory processes we highlight in this review.

Interactions among thyroid hormones and serum lipid levels in association with PCB exposure in the Mohawk Akwesasne population.

Alterations in thyroid function and serum lipid levels were assessed in relation to exposure to polychlorinated biphenyls (PCBs) and three chlorinated pesticides (DDE, hexachorobenzene and mirex) in a sample of Akwesasne Mohawk adults. This population is highly exposed to PCBs because of living in close proximity to three aluminum foundries that used PCBs as hydraulic fluids, which then contaminated local fish, wildlife, water, air and soils. The goal was to assess interactions between thyroid function (TSH, T3, T4 and fT4) and serum lipids (cholesterol, triglycerides and total serum lipids) in relation to concentrations of 101 PCB congeners and three chlorinated pesticides. Previous studies in this population have shown that elevated concentrations of PCBs resulted in suppression of thyroid function in adolescents, and increased risk of clinical hypothyroidism in adults, as well as an elevation in serum lipids. However in adjusted analyses of PCB concentrations of 703 adults we find only small and inconsistent associations between serum PCB levels and thyroid function. The most striking observations were strong significant positive associations between TSH and T3 with serum lipids and a negative association with fT4 in women. Because elevated serum lipids increase risks of other diseases the respective roles of thyroid hormones and PCBs in regulation of serum lipids requires additional study.

The Critical Importance of Molecular Biomarkers and Imaging in the Study of Electrohypersensitivity. A Scientific Consensus International Report.

Clinical research aiming at objectively identifying and characterizing diseases via clinical observations and biological and radiological findings is a critical initial research step when establishing objective diagnostic criteria and treatments. Failure to first define such diagnostic criteria may lead research on pathogenesis and etiology to serious confounding biases and erroneous medical interpretations. This is particularly the case for electrohypersensitivity (EHS) and more particularly for the so-called "provocation tests", which do not investigate the causal origin of EHS but rather the EHS-associated particular environmental intolerance state with hypersensitivity to man-made electromagnetic fields (EMF). However, because those tests depend on multiple EMF-associated physical and biological parameters and have been conducted in patients without having first defined EHS objectively and/or endpoints adequately, they cannot presently be considered to be valid pathogenesis research methodologies. Consequently, the negative results obtained by these tests do not preclude a role of EMF exposure as a symptomatic trigger in EHS patients. Moreover, there is no proof that EHS symptoms or EHS itself are caused by psychosomatic or nocebo effects. This international consensus report pleads for the acknowledgement of EHS as a distinct neuropathological disorder and for its inclusion in the WHO International Classification of Diseases.

Extremely low frequency electromagnetic fields and cancer: How source of funding affects results.

While there has been evidence indicating that excessive exposure to magnetic fields from 50 to 60 Hz electricity increases risk of cancer, many argue that the evidence is inconsistent and inconclusive. This is particularly the case regarding magnetic field exposure and childhood leukemia. A major goal of this study is to examine how source of funding influences the reported results and conclusions. Several meta-analyses dating from about 2000 all report significant associations between exposure and risk of leukemia. By examining subsequent reports on childhood leukemia it is clear that almost all government or independent studies find either a statistically significant association between magnetic field exposure and childhood leukemia, or an elevated risk of at least OR = 1.5, while almost all industry supported studies fail to find any significant or even suggestive association. A secondary goal of this report is to examine the level of evidence for exposure and elevated risk of various adult cancers. Based on pooled or meta-analyses as well as subsequent peer-reviewed studies there is strong evidence that excessive exposure to magnetic fields increases risk of adult leukemia, male and female breast cancer and brain cancer. There is less convincing but suggestive evidence for elevations in several other cancer types. There is less clear evidence for bias based on source of funding in the adult cancer studies. There is also some evidence that both paternal and maternal prenatal exposure to magnetic fields results in an increased risk of leukemia and brain cancer in offspring. When one allows for bias reflected in source of funding, the evidence that magnetic fields increase risk of cancer is neither inconsistent nor inconclusive. Furthermore adults are also at risk, not just children, and there is strong evidence for cancers in addition to leukemia, particularly brain and breast cancer.

Persistent organic pollutants as predictors of increased FSH:LH ratio in naturally cycling, reproductive age women.

Although several recent studies suggest endocrine disrupting compounds, such as polychlorinated biphenyls (PCBs), dichlorodiphenyldichloroethylene (p,p', DDE), and hexachlorobenzene (HCB), target different organs and systems in the body, their impact on female reproductive function in humans is not well characterized. We seek to determine the relationship between several known endocrine disrupting compounds and a marker of ovarian responsivity, the FSH:LH ratio (higher ratio indicates less ovarian responsivity). For this analysis, 169 naturally cycling women between 21 and 38 years of age completed interviews and had their blood drawn on day 3 of their menstrual cycle for analyses of toxicants, gonadal sex hormones (E2 and P4), and gonadotropins (FSH and LH). PCB congeners were classified into five groups based on their environmental persistence, distribution in human tissue, and toxicological action, reflecting the structure, mechanism, and known biological activity of individual PCB congeners. For every unit (ppb) increase in the level of the estrogenic PCB group, there was a 5-fold greater risk of a FSH:LH ratio ≥ 2, controlling for individual differences in age, percent body fat, cycle day 3 estradiol levels, parity, alcohol use and cigarette smoking in the past year (exp[ß] = 5; p = ≤0.01). PCB congeners identified as estrogenic were analyzed individually, and, of the 19 potentially estrogenic congeners, five were significantly, and positively related to an increased FSH:LH ratio. Four of these congeners are non-persistent, easily volatilize in the environment, and are easily metabolized, and hence, are indicative of very recent or current exposure. p,p'-DDE and HCB were not associated with FSH:LH ratio. We find a clinical indicator of ovarian responsivity, FSH:LH ratio, is associated with a specific group of estrogenic PCBs. These congeners may become airborne when they volatilize from dredged PCB-contaminated soil or from indoor PCB-containing window caulk and sealants in older buildings leading to inhalation exposure. PCB exposure, particularly to non-persistent, estrogenic congeners, may pose an unrecognized threat to female fecundity within the general population.

Exposure to perfluoroalkyl substances and associations with serum thyroid hormones in a remote population of Alaska Natives.

Perfluoroalkyl substances (PFASs) are known to accumulate in traditional food animals of the Arctic, and arctic indigenous peoples may be exposed via consumption of subsistence-harvested animals. PFASs are suspected of disrupting thyroid hormone homeostasis in humans. The aim of this study is to assess the relationship between serum PFASs and thyroid function in a remote population of Alaska Natives. Serum samples were collected from 85 individuals from St. Lawrence Island, Alaska. The concentrations of 13 PFASs, as well as free and total thyroxine (T4), free and total triiodothyronine (T3), and thyrotropin (TSH) were quantified in serum samples. The relationships between circulating concentrations of PFASs and thyroid hormones were assessed using multiple linear regression fit with generalized estimating equations. Several PFASs, including perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA), were positively associated with TSH concentrations when modeled individually. PFOS and PFNA were significantly associated with free T3 and PFNA was significantly associated with total T3 in models with PFAS*sex interactive terms; these associations suggested negative associations in men and positive associations in women. PFASs were not significantly associated with concentrations of free or total T4. Serum PFASs are associated with circulating thyroid hormone concentrations in a remote population of Alaska Natives. The effects of PFAS exposure on thyroid hormone homeostasis may differ between sexes.

Endocrine disrupting chemicals and ovulation: Is there a relationship?

Although the potential for endocrine disrupting chemicals (EDCs) to disrupt female fecundity is great, few studies have assessed the threat to human reproduction. This study investigates levels of organochlorines in relation to their impact on women's menstrual cycles and ovulatory status. To address concerns of the Akwesasne Mohawk community in upstate New York regarding well-established exposure to EDCs, women's fertility and reproductive health endpoints, we recruited 215 women between the ages of 21 and 38 years to measure menstrual cycle characteristics and levels of local pollutants. Of these, 155 women collected saliva over the course of their menstrual cycle allowing for analysis of estradiol and progesterone levels and the determination of ovulatory status in relationship to their serum pollutant levels. A subset of participants (15) who did not commence cycling within a month of their enrollment were not included in the analysis, hence reducing the sample size to 140 participants. Additionally, a lipid panel, estradiol and progesterone were assessed in serum on Day 3 of the menstrual cycle. Median cycle length for women in the sample was 29 days. After aligning the cycles, 110 women were considered ovulatory and 45 (29%) anovulatory. Concentrations of groups of more persistent PCBs congeners, HCB, and p,p'-DDE did not differ significantly with ovulatory status. However, a sub-group of low-chlorinated PCB congeners, considered to be estrogenic were significantly higher among anovulatory women. These findings suggest that certain EDC's, ubiquitous in our environment, may adversely affect menstrual cycles and thus have the capacity to impair reproductive function, including likelihood of conception.

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.

Early-life risk factors for chronic nonrespiratory diseases.

We have witnessed a change in disease patterns contributing to the global burden of disease, with a shift from early childhood deaths due to the classic infectious communicable diseases to years lived with disability from chronic noncommunicable diseases. In both developing and developed countries, the years lived with disability attributable to chronic disease have increased: cardiovascular diseases by 17.7%; chronic respiratory disease by 8.5%; neurological conditions by 12.2%; diabetes by 30.0%; and mental and behavioural disorders by 5.0% over the past 20 years. Recognition of the contribution made by adverse environmental exposures in early life to noncommunicable diseases in later life is increasing. These early-life exposures appear to contribute to both chronic respiratory and chronic nonrespiratory diseases. In this State of the Art article, we aim to examine early-life environmental exposures that have an epidemiological association with chronic nonrespiratory diseases, such as obesity and type II diabetes, cardiovascular disease, and neurocognitive and behavioural problems. We will highlight the potential overlap in environmental risks with respiratory diseases, and point out knowledge gaps and research opportunities.

Environmental health and justice and the right to research: institutional review board denials of community-based chemical biomonitoring of breast milk.

Recently, conflicts and challenges have emerged regarding environmental justice and research ethics for some indigenous communities. Alaska Community Action on Toxics (ACAT) responded to community requests for breast milk biomonitoring and conceived the Breast Milk Pilot Study (BMPS). Despite having community support and federal and private funding, the BMPS remains incomplete due to repeated disapprovals by the Alaska Area IRB (Institutional Review Board). In this commentary, we explore the consequences of years of IRB denials, in terms of health inequalities, environmental justice, and research ethics. We highlight the greater significance of this story with respect to research in Alaska Native communities, biomonitoring, and global toxics regulation. We offer suggestions to community-based researchers conducting biomonitoring projects on how to engage with IRBs in order to cultivate reflective, context-based research ethics that better consider the needs and concerns of communities.

Inhalation of Polychlorinated Biphenyls (PCB) Produces Hyperactivity in Rats.

Attention deficit hyperactivity disorder (ADHD) is a serious behavioral syndrome seen in children, and more common in males than females. There is increasing evidence that prenatal and/or early life exposure to persistent organic pollutants (POP) such as polychlorinated biphenyls (PCB) is associated with increased risk of ADHD occurrence. While PCB exposure is usually attributed to ingestion of contaminated food, recent reports of elevated PCB concentrations in indoor air, especially in schools, raised concern regarding inhalation as an important route of exposure to PCB with consequent effects on neurobehavior. The effects of exposure to air contaminated with Aroclor 1248 or contaminated sediment (SED) from the St. Lawrence River were examined on operant behavior of male and female Sprague-Dawley rats. Data showed that relative to controls, vapor-phase inhalation of PCB, whether from blowing air over Aroclor 1248 or from blowing air over sediment contaminated with PCB, resulted in hyperactivity and impatience in rats, more pronounced in males than females. These results are consistent with the hypothesis that inhalation of PCB may contribute to behavioral abnormalities in children.

Persistent Organochlorine Pesticide Exposure Related to a Formerly Used Defense Site on St. Lawrence Island, Alaska: Data from Sentinel Fish and Human Sera.

St. Lawrence Island, Alaska, is the largest island in the Bering Sea, located 60 km from Siberia. The island is home to approximately 1600 St. Lawrence Island Yupik residents who live a subsistence way of life. Two formerly used defense sites (FUDS) exist on the island, one of which, Northeast Cape, has been the subject of a $123 million cleanup effort. Environmental monitoring demonstrates localized soil and watershed contamination with polychlorinated biphenyls (PCB), organochlorine (OC) pesticides, mercury, and arsenic. This study examined whether the Northeast Cape FUDS is a source of exposure to OC pesticides. In total, 71 serum samples were collected during site remediation from volunteers who represented three geographic regions of the island. In addition, ninespine stickleback (Pungitius pungitius) and Alaska blackfish (Dallia pectoralis) were collected from Northeast Cape after remediation to assess continuing presence of OC pesticides. Chlordane compounds, DDT compounds, mirex, and hexachlorobenzene (HCB) were the most prevalent and present at the highest concentrations in both fish tissues and human serum samples. After controlling for age and gender, activities near the Northeast Cape FUDS were associated with an increase in serum HCB as compared to residents of the farthest village from the site. Positive but nonsignificant relationships for sum-chlordane and sum-DDT were also found. Organochlorine concentrations in fish samples did not show clear geographic trends, but appear elevated compared to other sites in Alaska. Taken together, data suggest that contamination of the local environment at the Northeast Cape FUDS may increase exposure to select persistent OC pesticides.

Exposure to and health effects of volatile PCBs.

INTRODUCTION: Polychlorinated biphenyls (PCBs) are persistent, lipophilic contaminants that are known to increase risk of a number of human diseases. Although ingestion of animal fats is a major route of exposure, there is increasing evidence that inhalation of vapor-phase PCBs is also important and may be as or even more important than ingestion under some circumstances. METHODS: The evidence that inhalation of PCBs may cause cancer, heart disease, hypertension, and diabetes is reviewed and presented in this report. RESULTS: PCBs are known human carcinogens. A husband and wife, occupationally required to 'smell' PCB-containing oils, both developed thyroid cancer, malignant melanoma/severely melanocytic dysplastic nevus (a precursor to malignant melanoma) and the husband, a non-smoker, developed and died of lung cancer. The serum of both had highly elevated concentrations of lower chlorinated, volatile PCB congeners. In other studies, residents living near PCB-containing hazardous waste sites, and thus breathing PCB-contaminated air, have elevated rates of hospitalization for cardiovascular disease, hypertension, diabetes and reduced cognitive performance, whereas other studies in defined populations show that there is an elevated risk of all of these diseases in individuals with elevated serum PCBs. CONCLUSIONS: These results are consistent with the conclusion that inhaled PCBs can increase risk of cancer, cardiovascular disease, hypertension, diabetes and reduce cognitive function.

Association between hospital discharge rate for female breast cancer and residence in a zip code containing hazardous waste sites.

BACKGROUND: Exposure to chemicals plays a role in risk of breast cancer. However, possible associations between risk of breast cancer and residential proximity to hazardous waste sites (HWSs) have not been reported. METHODS: We determined rates of hospital discharge with a diagnosis of female breast cancer in relation to residence in a zip code containing HWSs in New York State (NYS) after adjustment for ethnicity, age, income and urbanicity. Waste exposure was assessed by both the number of waste sites and the type of contaminants. Negative binomial regression was used to test the associations. RESULTS: After controlling for confounders, the hospital discharge rate of breast cancer for women living in zip codes having four or more HWSs or in zip codes having one HWS increased significantly (at the 0.05 level) by 9.1% and 6.4%, as compared to those living in a zip code with no HWS. The association for women living in zip codes having two or three HWSs was not significant. This indicates that the extent of exposure cannot be assessed solely by the number of waste sites. The discharge rate for women living in zip codes containing at least one volatile organic compound (VOC) waste site was significantly increased 5.6% as compared to those living in a zip code without any HWS, while the increases were not significant for women living in zip codes containing waste sites with persistent organic pollutants (POPs) or other contaminants. The significant associations were stronger for African American than Caucasian women and stronger in more urbanized than in rural areas. CONCLUSIONS: Residence within a geographic area (defined by zip codes) that includes a hazardous waste site with VOCs is significantly associated with an increased rate of hospitalization for breast cancer, and the association is stronger for African American than Caucasian women and stronger in more urbanized than in rural areas after adjustment for the confounders.

Risk-benefit of consuming Lake Erie fish.

BACKGROUND: Consumption of fish is promoted as a healthy way to obtain essential fatty acids (EFA) in the diet, yet the risk of ingesting harmful contaminants remains a concern. A recent study concluded that the risk-benefit of consuming fish from the North American Laurentian Great Lakes, which sustain important commercial and recreational fisheries, is currently unclear. We report the fatty acid (FA) content in skin-off fillets of fifteen fish species from Lake Erie and assess whether recommended dietary requirements for two EFA (EPA and DHA) can be met by safely consuming Lake Erie fishes, as an example of a risk-benefit analysis. METHODS: A total of 146 samples were analyzed for FA and contaminant content. A simulated fish consumption advisory (maximum recommended number of meals per month, up to 32) was calculated for each sample, and used to calculate the maximum amount of EPA+DHA that would be consumed if the consumption advisory was followed. RESULTS: All fifteen species had nutritionally desirable PUFA:SAFA (>0.4) and n-3:n-6 (>1). Large, fatty species had the highest EPA+DHA content, but had the most restrictive consumption advisories due to high PCB concentrations. To minimize contaminant exposure while maximizing EPA+DHA intake, consumers should consider small lake whitefish and lake trout, small panfish species, and/or walleye. However, very few species had an EPA+DHA content sufficient to safely meet the highest dietary guidelines while following advisories. CONCLUSIONS: Consumption of certain Lake Erie fish, an important recreational and commercial fishery, within the limits of our simulated fish consumption advisories, can be a good supplemental source of beneficial n-3 long chain PUFA.