Ambient Air Pollutants and Olfaction among Women 50-79 Years of Age from the Sister Study.

BACKGROUND: Poor olfaction is common in older adults and may have profound adverse implications on their health. However, little is known about the potential environmental contributors to poor olfaction. OBJECTIVE: We investigated ambient fine particulate matter [PM ≤2.5µm in aerodynamic diameter (PM2.5)] and nitrogen dioxide (NO2) in relation to poor olfaction in middle-aged to older women. METHODS: The Sister Study is a nationwide cohort of 50,884 women in the United States with annual average air pollutant exposures estimated based on participants' residences from enrollment (2003-2009) through 2017. This analysis was limited to 3,345 women, 50-79 years of age as of January 2018, who completed the Brief Smell Identification Test (B-SIT) in 2018-2019. Poor olfaction was defined as a B-SIT score of ≤9 in the primary analysis. We conducted multivariable logistic regressions, accounting for covariates and study sampling design. RESULTS: Overall, we found little evidence for associations of air pollutants with poor olfaction. The odds ratio (OR) and 95% confidence interval (CI) of poor olfaction for each interquartile range (IQR) increment of air pollutants in 2006 were 1.03 (95% CI: 0.91, 1.17) for PM2.5 (per 3.3 µg/m3) and 1.08 (95% CI: 0.96, 1.22) for NO2 (per 5.7 ppb). Results were similar in the analyses using the most recent (2017) or the cumulative average (2006-2017) air pollutant exposure data. Secondary analyses suggested potential association in certain subgroups. The OR per IQR was 1.35 (95% CI: 1.11, 1.65) for PM2.5 among younger participants (<54.2 years of age) and 1.87 (95% CI: 1.29, 2.71) for NO2 among current smokers. DISCUSSION: This study did not find convincing evidence that air pollutants have lasting detrimental effects on the sense of smell of women 50-79 years of age. The subgroup analyses are exploratory, and the findings need independent confirmation. https://doi.org/10.1289/EHP12066.

Association between spill-related exposure to fine particulate matter and peripheral motor and sensory nerve function among oil spill response and cleanup workers following the Deepwater Horizon oil spill.

BACKGROUND: Burning/flaring of oil/gas during the Deepwater Horizon oil spill response and cleanup (OSRC) generated high concentrations of fine particulate matter (PM2.5). Personnel working on the water during these activities may have inhaled combustion products. Neurologic effects of PM2.5 have been reported previously but few studies have examined lasting effects following disaster exposures. The association of brief, high exposures and adverse effects on sensory and motor nerve function in the years following exposure have not been examined for OSRC workers. OBJECTIVES: We assessed the relationship between exposure to burning/flaring-related PM2.5 and measures of sensory and motor nerve function among OSRC workers. METHODS: PM2.5 concentrations were estimated from Gaussian plume dispersion models and linked to self-reported work histories. Quantitative measures of sensory and motor nerve function were obtained 4-6 years after the disaster during a clinical exam restricted to those living close to two clinics in Mobile, AL or New Orleans, LA (n = 3401). We obtained covariate data from a baseline enrollment survey and a home visit, both in 2011-2013. The analytic sample included 1186 participants. RESULTS: We did not find strong evidence of associations between exposure to PM2.5 and sensory or motor nerve function, although there was a suggestion of impairment based on single leg stance among individuals with high exposure to PM2.5. Results were generally consistent whether we examined average or cumulative maximum exposures or removed individuals with the highest crude oil exposures to account for co-pollutant confounding. There was no evidence of exposure-response trends. IMPACT STATEMENT: Remediating environmental disasters is essential for long-term human and environmental health. During the Deepwater Horizon oil spill disaster, burning and flaring of oil and gas were used to remove these pollutants from the environment, but led to potentially high fine particulate matter exposures for spill response workers working on the water. We investigate the potential adverse effects of these exposures on peripheral nerve function; understanding the potential health harm of remediation tactics is necessary to inform future clean up approaches and protect human health.

Exposure to volatile hydrocarbons and neurologic function among oil spill workers up to 6 years after the Deepwater Horizon disaster.

BACKGROUND: During the 2010 Deepwater Horizon (DWH) disaster, oil spill response and cleanup (OSRC) workers were exposed to toxic volatile components of crude oil. Few studies have examined exposure to individual volatile hydrocarbon chemicals below occupational exposure limits in relation to neurologic function among OSRC workers. OBJECTIVES: To investigate the association of several spill-related chemicals (benzene, toluene, ethylbenzene, xylene, n-hexane, i.e., BTEX-H) and total petroleum hydrocarbons (THC) with neurologic function among DWH spill workers enrolled in the Gulf Long-term Follow-up Study. METHODS: Cumulative exposure to THC and BTEX-H across the oil spill cleanup period were estimated using a job-exposure matrix that linked air measurement data to detailed self-reported DWH OSRC work histories. We ascertained quantitative neurologic function data via a comprehensive test battery at a clinical examination that occurred 4-6 years after the DWH disaster. We used multivariable linear regression and modified Poisson regression to evaluate relationships of exposures (quartiles (Q)) with 4 neurologic function measures. We examined modification of the associations by age at enrollment (<50 vs. ≥50 years). RESULTS: We did not find evidence of adverse neurologic effects from crude oil exposures among the overall study population. However, among workers ≥50 years of age, several individual chemical exposures were associated with poorer vibrotactile acuity of the great toe, with statistically significant effects observed in Q3 or Q4 of exposures (range of log mean difference in Q4 across exposures: 0.13-0.26 µm). We also observed suggestive adverse associations among those ≥ age 50 years for tests of postural stability and single-leg stance, although most effect estimates did not reach thresholds of statistical significance (p < 0.05). CONCLUSIONS: Higher exposures to volatile components of crude oil were associated with modest deficits in neurologic function among OSRC workers who were age 50 years or older at study enrollment.

Fine particulate matter and incident coronary heart disease events up to 10 years of follow-up among Deepwater Horizon oil spill workers.

BACKGROUND: During the 2010 Deepwater Horizon (DWH) disaster, in-situ burning and flaring were conducted to remove oil from the water. Workers near combustion sites were potentially exposed to burning-related fine particulate matter (PM2.5). Exposure to PM2.5 has been linked to increased risk of coronary heart disease (CHD), but no study has examined the relationship among oil spill workers. OBJECTIVES: To investigate the association between estimated PM2.5 from burning/flaring of oil/gas and CHD risk among the DWH oil spill workers. METHODS: We included workers who participated in response and cleanup activities on the water during the DWH disaster (N = 9091). PM2.5 exposures were estimated using a job-exposure matrix that linked modelled PM2.5 concentrations to detailed DWH spill work histories provided by participants. We ascertained CHD events as the first self-reported physician-diagnosed CHD or a fatal CHD event that occurred after each worker's last day of burning exposure. We estimated hazard ratios (HR) and 95% confidence intervals (95%CI) for the associations between categories of average or cumulative daily maximum PM2.5 exposure (versus a referent category of water workers not near controlled burning) and subsequent CHD. We assessed exposure-response trends by examining continuous exposure parameters in models. RESULTS: We observed increased CHD hazard among workers with higher levels of average daily maximum exposure (low vs. referent: HR = 1.26, 95% CI: 0.93, 1.70; high vs. referent: HR = 2.11, 95% CI: 1.08, 4.12; per 10 µg/m3 increase: HR = 1.10, 95% CI: 1.02, 1.19). We also observed suggestively elevated HRs among workers with higher cumulative daily maximum exposure (low vs. referent: HR = 1.19, 95% CI: 0.68, 2.08; medium vs. referent: HR = 1.38, 95% CI: 0.88, 2.16; high vs. referent: HR = 1.44, 95% CI: 0.96, 2.14; per 100 µg/m3-d increase: HR = 1.03, 95% CI: 1.00, 1.05). CONCLUSIONS: Among oil spill workers, exposure to PM2.5 from flaring/burning of oil/gas was associated with increased risk of CHD.

Fossil-fuel and combustion-related air pollution and hypertension in the Sister Study.

Hypertension is a leading risk factor for disease burden, with more than 200 million disability-adjusted life-years attributed to high blood pressure in 2015. While outdoor air pollution is associated with cardiovascular disease, the joint effect of exposure to air pollution from combustion products on hypertension has rarely been studied. We conducted a cross-sectional analysis to explore the association between combustion-related air pollution and hypertension. Census-tract levels of ambient concentrations of nine fossil-fuel and combustion-related air toxics (biphenyl, naphthalene, polycyclic organic matter, diesel emissions, 1,3-butadiene, acetaldehyde, benzene, acrolein, and formaldehyde) from the 2005 National Air Toxics Assessment database and NO2 from 2005 monitoring data were linked to baseline residential addresses of 47,467 women in the Sister Study cohort. Hypertension at enrollment (2003-2009) was defined as high systolic (≥140 mm Hg) or diastolic (≥90 mm Hg) blood pressure or taking antihypertensive medication. We used log-binomial regression and quantile-based g-computation to estimate the individual and joint effects of fossil-fuel and combustion-related air pollution on hypertension. Comparing the highest to lowest quartiles, diesel emissions (prevalence ratio (PR) = 1.05, 95% confidence interval (CI) = 1.01,1.08), 1,3-butadiene (PR = 1.04, 95%CI = 1.00,1.07), acetaldehyde (PR = 1.08, 95%CI = 1.04,1.12), benzene (PR = 1.05, 95%CI = 1.02,1.08), formaldehyde (PR = 1.08, 95%CI = 1.04,1.11), and NO2 (PR = 1.08, 95%CI = 1.05,1.12) were individually associated with higher prevalence of hypertension. The PR for the joint effect of increasing all ambient air toxics and NO2 by one quartile was 1.02 (95%CI = 1.01,1.04). Associations varied by race/ethnicity, with stronger associations observed among women reporting races/ethnicities (Hispanic/Latina, non-Hispanic Black and other) other than non-Hispanic White. In conclusion, we found that air pollution from fossil fuel and combustion may be a risk factor for hypertension.

Assessment of Self-reported Sense of Smell, Objective Testing, and Associated Factors in Middle-aged and Older Women.

Importance: Poor olfaction is common in older adults and signifies multiple adverse health outcomes, but it often goes unrecognized. Objective: To characterize the self-awareness of poor olfaction in women, including its prevalence, associated factors, reporting reliability, validity against an objective test, and factors associated with validity. Design, Setting, and Participants: These cross-sectional survey data and a case-control subsample were taken from the National Institute of Environmental Health Sciences' Sister Study. Of 41 118 participants (aged 41-85 years) who reported olfaction in 2014 through 2016, 3406 (aged 50-79 years) reported olfaction again in 2018 through 2019 and completed the 12-item Brief Smell Identification Test, version A, including 2353 women who self-reported poor olfaction in 2014 through 2016 and 1053 women who reported normal olfaction. Data analyses were performed between May 28, 2021, and December 23, 2021. Main Outcomes and Measures: Self-reported (yes/no) and objectively tested poor olfaction defined as a Brief Smell Identification Test score of 9 or lower. Multivariable logistic regressions were used to assess factors that might be associated with the prevalence and reporting accuracy of self-reported olfaction. In subsample analyses, the sampling strategy was accounted for to extrapolate data to eligible cohort samples. Results: Of the 41 118 women (mean [SD] age, 64.3 [8.7] years) included in the analysis, 3322 (8.1%) self-reported poor olfaction. Higher prevalence was associated with older age, not being married, current smoking status, frequent coffee drinking, overweight or obesity, less than optimal health, Parkinson disease, cognitive impairment, depression, anxiety, and seasonal allergy, whereas a lower prevalence was associated with non-Hispanic Black race and physical activity. In the subsample analyses, olfaction status reported 3 years apart showed a modest agreement (κ, 0.56; 95% CI, 0.51-0.61). The prevalence of objectively tested poor olfaction was 13.3% (95% CI, 11.5%-15.0%), and in contrast with self-reports, it was twice as high in non-Hispanic Black women as in non-Hispanic White women (24.5% vs 12.5%). Compared with objective tests, self-reports showed a low sensitivity (22.6%; 95% CI, 19.6%-25.6%), especially in non-Hispanic Black women (12.4%; 95% CI, 7.0%-17.8%). The specificity was uniformly high (>90%). Among participants who reported poor olfaction, higher odds of true vs false positives were associated with age older than 60 years (60-64 years old, 1.68; 95% CI, 1.51-1.87; 65-69 years old, 2.26; 95% CI, 2.03-2.51; 70-74 years old, 3.34; 95% CI, 3.00-3.73; ≥75 years old, 5.17; 95% CI, 4.43-6.03), non-Hispanic Black race (2.00; 95% CI, 1.70-2.36), no college education (1.34; 95% CI, 1.22-1.48), underweight (1.40; 95% CI, 1.04-1.88), fair or poor health (1.37; 95% CI, 1.22-1.54), and Parkinson disease (7.60; 95% CI, 5.60-10.32). Among those with objectively tested poor olfaction, lower odds of true positives vs false negatives were associated with Black race (0.46; 95% CI, 0.25-0.86). Conclusions and Relevance: In this case-control study, the self-awareness and reporting accuracy of poor olfaction in middle-aged and older women were low, particularly in non-Hispanic Black women. Given its potential health implications, awareness of this common sensory deficit should be raised.

Ambient particulate matter, ozone, and neurologic symptoms in U.S. Gulf states adults.

Research on neurologic effects of air pollution has focused on neurodevelopment or later-life neurodegeneration; other effects throughout adulthood have received less attention. We examined air pollution levels and neurologic symptoms among 21,467 adults in US Gulf Coast states. We assigned exposure using Environmental Protection Agency estimates of daily ambient particulate matter 2.5 (PM2.5) and ozone. Gulf Long-term Follow-up Study participants reported neurologic symptoms at enrollment (2011-2013). We estimated cross-sectional associations between each air pollutant and prevalence of "any" neurologic, central nervous system (CNS), or peripheral nervous system (PNS) symptoms. Ambient PM2.5 was consistently associated with prevalence of neurologic symptoms. The highest quartile of 30-day PM2.5 was associated with any neurologic symptom (prevalence ratio [PR] = 1.16; 95% confidence interval [CI] = 1.09, 1.23) and there were increasing monotonic relationships between 30-day PM2.5 and each symptom category (P-trend ≤ 0.01). Associations with PM2.5 were slightly stronger among nonsmokers and during colder seasons. The highest quartile of 7-day ozone was associated with increased prevalence of PNS symptoms (PR = 1.09; 95% CI = 1.00, 1.19; P-trend = 0.03), but not with other outcomes. Ozone concentrations above regulatory levels were suggestively associated with neurologic symptoms (PR = 1.06; 95% CI = 0.99, 1.14). Mutual adjustment in co-pollutant models suggests that PM2.5 is more relevant than ozone in relation to prevalence of neurologic symptoms.

Association of neighborhood deprivation with pulmonary function measures among participants in the Gulf Long-Term Follow-up Study.

INTRODUCTION: Individual-level socioeconomic status (SES) has been shown to be an important determinant of lung function. Neighborhood level SES factors may increase psychological and physiologic stress and may also reflect other exposures that can adversely affect lung function, but few studies have considered neighborhood factors. OBJECTIVE: Our aim was to assess the association between neighborhood-level SES and lung function. METHODS: We cross-sectionally analyzed 6168 spirometry test results from participants in the Gulf long-term Follow-up Study, a large cohort of adults enrolled following the largest maritime oil spill in US history. Outcomes of interest included the forced expiratory volume in 1 s (FEV1; mL), the forced vital capacity (FVC; mL), and the FEV1/FVC ratio (%). Neighborhood deprivation was measured by linking participant home addresses to an existing Area Deprivation Index (ADI) and categorized into quartiles. Individual-level SES measures were collected at enrollment using a structured questionnaire and included income, educational attainment, and financial strain. We used multilevel regression to estimate associations between ADI quartiles and each lung function measure. RESULTS: Greater neighborhood deprivation was associated with lower FEV1: ßQ2vsQ1: -30 mL (95% CI: -97, 36), ßQ3vsQ1: -70 mL (95% CI: -135, -4) and ßQ4vsQ1: -104 mL (95% CI: -171, -36). FVC showed similar patterns of associations with neighborhood deprivation. No associations with the FEV1/FVC ratio were observed. CONCLUSION: Neighborhood deprivation, a measure incorporating economic and other stressors, was associated with lower FEV1 and FVC, with magnitudes of associations reaching clinically meaningful levels. The impact of this neighborhood SES measure persisted even after adjustment for individual-level SES factors.

Selenium modifies associations between multiple metals and neurologic symptoms in Gulf states residents.

BACKGROUND: Metals have been shown to have a wide range of neurologic effects across the life course, but most studies consider neurodevelopment or neurodegenerative diseases in older adults. We investigated exposure to metals during adulthood in association with subclinical neurologic endpoints, considering the metals individually and as a mixture, and potential interactions among exposures. METHODS: We measured blood levels of cadmium, lead, mercury, manganese, and selenium in 1007 Gulf state residents and estimated cross-sectional associations between ranked levels of blood metals and the presence of self-reported neurologic symptoms. Single pollutant models were mutually adjusted for other metals and we used quantile g-computation to evaluate associations with exposure to the combined mixture. In stratified analyses, we assessed heterogeneity by smoking and blood selenium. RESULTS: The highest quartile of cadmium was associated with a higher prevalence of central nervous system symptoms (prevalence ratio [PR] = 1.50; 95% confidence interval [CI] = 1.13, 1.99), with stronger associations among nonsmokers (PR = 1.63; 95% CI = 1.11, 2.38) and those with low selenium (PR = 2.29, 95% CI = 1.50, 3.49). Selenium also modified associations between lead and peripheral nervous system symptoms, with increased symptoms in the low selenium group at all quartiles of exposure (P-trend = 0.07). Conversely, those with the highest co-exposure to mercury and selenium had reduced neurologic symptoms (PR = 0.73, 95% CI = 0.55, 0.96). Results of the mixture analysis were consistent with single chemical results. CONCLUSIONS: Cadmium exhibited the most consistent relationship with increased neurologic symptoms, though lead was an important exposure in subgroup analyses. Selenium may modify subclinical neurotoxic effects of metals at non-occupational levels in adults.

Herbicide, fumigant, and fungicide use and breast cancer risk among farmers' wives.

Evidence from epidemiologic and laboratory studies relating pesticides to breast cancer risk is inconsistent. Women engaging in agricultural work or living in agricultural areas may experience appreciable exposures to a wide range of pesticides, including herbicides, fumigants, and fungicides. METHODS: We examined exposure to herbicides, fumigants, and fungicides in relation to breast cancer risk among farmers' wives with no prior history of breast cancer in the Agricultural Health Study. Women provided information on pesticide use, demographics, and reproductive history at enrollment (1993-1997) and at a 5-year follow-up interview. We used Cox proportional hazards regression to estimate associations (hazard ratios [HRs] and 95% confidence intervals [CIs]) between the women's and their husbands' self-reported use of individual pesticides and incident breast cancer risk. RESULTS: Out of 30,594 women, 38% reported using herbicides, fumigants, or fungicides and 1,081 were diagnosed with breast cancer during a median 15.3 years of follow-up. We found elevated risk in relation to women's ever use of the fungicide benomyl (HR = 1.6; 95% CI = 0.9, 2.7) and the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) (HR = 1.6; 95% CI = 0.8, 3.1) and to their husbands' use of the herbicide 2-(2,4,5-trichlorophenoxy) propionic acid (2,4,5-TP) (HR = 1.5; 95% CI = 0.9, 2.7). We observed few other chemical associations and little evidence of differential risk by tumor estrogen receptor status or linear exposure-response relationships. CONCLUSION: We did not observe clear excesses between use of specific pesticides and breast cancer risk across exposure metrics, although we did observe elevated risk associated with women's use of benomyl and 2,4,5-T and husbands' use of 2,4,5-TP.

Blood BTEXS and heavy metal levels are associated with liver injury and systemic inflammation in Gulf states residents.

INTRODUCTION: Exposures to volatile organic compounds and metals have previously been associated with liver diseases including steatohepatitis, although more data are needed. Benzene, toluene, ethylbenzene, xylenes, styrene (BTEXS) and metals were measured in blood samples collected between May 2012-July 2013 from volunteers participating in home visits for the Gulf Long-term Follow-up (GuLF) Study. This cross-sectional analysis evaluates associations of exposure biomarkers with serum liver injury and adipocytokine biomarkers in a sample of 214 men. METHODS: Adult nonsmoking men without a history of liver disease or heavy alcohol consumption were included. The serologic disease biomarkers evaluated were the hepatocellular injury biomarker, cytokeratin 18 [whole (CK18 M65) and caspase-cleaved fragment (CK18 M30)]; and adipocytokines. Confounder-adjusted beta coefficients were determined using linear regression models for the overall sample (primary endpoints) and for obesity-classified sub-groups (secondary endpoints). A product interaction term between the exposure of interest and a dichotomized indicator of obesity was included to determine the disease modifying effects of obesity on the biomarker associations. RESULTS: The study sample was 57% white and 51% obese. In the overall sample, lead was positively associated with CK18 M30 (ß = 21.7 ± 6.0 (SE), p = 0.0004); IL-1ß (ß = 32.8 ± 5.2, p < 0.0001); IL-6 (ß = 72.8 ± 18.3, p = 0.0001); and IL-8 (ß = 140.8 ± 42.2, p = 0.001). Cadmium exposures were associated with increased IL-1ß (ß = 77.8 ± 26.3, p = 0.003) and IL-8 (ß = 419.5 ± 201.2, p = 0.04). There were multiple significant interactions between obesity and exposure to lead, cadmium, benzene and toluene in relation to outcome biomarkers. Among obese participants (n = 108), benzene, lead, and cadmium were each positively associated with CK18 M30, IL-1ß, IL-6, and IL-8. In obese subjects, lead was also inversely associated with leptin, and toluene was positively associated with IL-1ß. CONCLUSION: For the overall sample, heavy metal exposures were associated with liver injury (lead only) and/or systemic inflammation (lead and cadmium). Obesity modified the associations between BTEXS and heavy metal exposures on several of the outcome variables. In the obesity subgroup, liver injury was positively associated with lead, cadmium and benzene exposures; systemic inflammation was increased with lead, cadmium, benzene, and toluene exposures; and leptin was inversely associated with lead exposures. The cross-sectional design of this study makes it difficult to determine causality, and all results should be interpreted cautiously. Nonetheless, the potential impact of exposures to lead, cadmium, benzene and toluene in steatohepatitis, an obesity-associated inflammatory liver disease, warrants further investigation.

Blood BTEX levels and neurologic symptoms in Gulf states residents.

BACKGROUND: The chemicals benzene, toluene, ethylbenzene, and xylenes (BTEX) are neuroactive. Exposures often co-occur because they share common sources. We examined neurologic effects of environmental BTEX exposure among U.S. Gulf coast residents taking into account concomitant exposures. METHODS: We measured blood concentrations of BTEX in 690 Gulf state residents. Neurologic symptoms were ascertained via telephone interview. We used log-binomial regression to estimate associations between blood BTEX levels and self-reported neurologic symptoms independently for the presence of any neurologic, central (CNS), or peripheral nervous system (PNS) symptoms. We estimated associations in single chemical models mutually adjusted for co-occurring BTEX and used weighted quantile sum regression to model associations between the combined BTEX mixture and neurologic symptoms. RESULTS: Half (49%) of participants reported at least one neurologic symptom. Each BTEX chemical was associated with increased CNS and PNS symptoms in single-chemical models comparing the highest to lowest quartile of exposure. After adjusting for coexposures, benzene was associated with CNS symptoms among all participants (PR = 2.13, 95% CI: 1.27, 3.57) and among nonsmokers (PR = 2.30, 95% CI: 1.35, 3.91). After adjusting for coexposures, associations with toluene were apparent only for reporting multiple PNS symptoms (PR = 2.00, 95% CI: 0.96, 4.16). In mixture analyses, a one-quartile increase in BTEX exposure was associated with neurologic symptoms (OR = 1.47, 95% CI: 1.11, 1.98). The weighted quantile sum index weighted benzene most heavily, which was consistent with single chemical analyses. CONCLUSIONS: Increasing blood benzene concentration was associated with increased prevalence of CNS symptoms. In this sample, BTEX-associated neurologic effects are likely driven by exposure to benzene and, to a lesser extent, toluene.

Environmental Styrene Exposure and Sensory and Motor Function in Gulf Coast Residents.

BACKGROUND: Although styrene is an established neurotoxicant at occupational exposure levels, its neurotoxicity has not been characterized in relation to general population exposures. Further, occupational research to date has focused on central nervous system impairment. OBJECTIVE: We assessed styrene-associated differences in sensory and motor function among Gulf coast residents. METHODS: We used 2011 National Air Toxics Assessment estimates of ambient styrene to determine exposure levels for 2,956 nondiabetic Gulf state residents enrolled in the Gulf Long-term Follow-up Study, and additionally measured blood styrene concentration in a subset of participants 1 to 2 y after enrollment ([Formula: see text]). Participants completed an enrollment telephone interview and a comprehensive test battery to assess sensory and motor function during a clinical follow-up exam 2 to 4 y later. Detailed covariate information was ascertained at enrollment via telephone interview. We used multivariate linear regression to estimate continuous differences in sensory and motor function, and log-binomial regression to estimate prevalence ratios for dichotomous outcomes. We estimated associations of both ambient and blood styrene exposures with sensory and motor function, independently for five unique tests. RESULTS: Those participants in the highest 25% vs. lowest 75% of ambient exposure and those in the highest 10% vs. lowest 90% of blood styrene had slightly diminished visual contrast sensitivity. Mean vibrotactile thresholds were lower among those in the highest vs. lowest quartile of ambient styrene and the highest 10% vs. lowest 90% of blood styrene ([Formula: see text] log microns; 95% CI: [Formula: see text], [Formula: see text] and [Formula: see text] log microns; 95% CI: [Formula: see text], [Formula: see text], respectively). The highest vs. lowest quartile of ambient styrene was associated with significantly poorer postural stability, and (unexpectedly) with significantly greater grip strength. DISCUSSION: We observed associations between higher styrene exposure and poorer visual, sensory, and vestibular function, though we did not detect associations with reduced voluntary motor system performance. Associations were more consistent for ambient exposures, but we also found notable associations with measured blood styrene. https://doi.org/10.1289/EHP3954.

Determinants of environmental styrene exposure in Gulf coast residents.

BACKGROUND: In a previous study of exposure to oil-related chemicals in Gulf coast residents, we measured blood levels of volatile organic compounds. Levels of styrene were substantially elevated compared to a nationally representative sample. We sought to identify factors contributing to these levels, given the opportunities for styrene exposure in this community. METHODS: We measured blood styrene levels in 667 Gulf coast residents and compared participants' levels of blood styrene to a nationally representative sample. We assessed personal and environmental predictors of blood styrene levels using linear regression and predicted the risk of elevated blood styrene (defined as above the National Health and Nutrition Examination Survey 95th percentile) using modified Poisson regression. We assessed exposure to styrene using questionnaire data on recent exposure opportunities and leveraged existing databases to assign ambient styrene exposure based on geocoded residential location. RESULTS: These Gulf coast residents were 4-6 times as likely as the nationally representative sample to have elevated blood styrene levels. The change in styrene (log ng/mL) was 0.42 (95% CI: 0.34, 0.51) for smoking, 0.34 (0.09, 0.59) for time spent in vehicles and 1.10 (0.31, 1.89) for boats, and -0.41 (-0.73, -0.10) for fall/winter blood draws. Residential proximity to industrial styrene emissions did not predict blood styrene levels. Ambient styrene predicted elevated blood styrene in subgroups. CONCLUSIONS: Personal predictors of increasing blood styrene levels included smoking, vehicle emissions, and housing characteristics. There was a suggestive association between ambient and blood styrene. Our measures of increased regional exposure opportunity do not fully explain the observed elevated blood styrene levels in this population.

Environmental styrene exposure and neurologic symptoms in U.S. Gulf coast residents.

BACKGROUND: Styrene is an established neurotoxicant at occupational levels, but effects at levels relevant to the general population have not been studied. We examined the neurologic effects of environmental styrene exposure among U.S. Gulf coast residents. METHODS: We used National Air Toxics Assessment (NATA) 2011 estimates of ambient styrene concentrations to assign exposure levels for 21,962 non-diabetic Gulf state residents, and additionally measured blood styrene concentration in a subset of participants (n = 874). Neurologic symptoms, as well as detailed covariate information, were ascertained via telephone interview. We used log-binomial regression to estimate prevalence ratios (PR) and 95% confidence intervals (95% CI) for cross-sectional associations between both ambient and blood styrene levels and self-reported neurologic symptoms. We estimated associations independently for ten unique symptoms, as well as for the presence of any neurologic, central nervous system (CNS), or peripheral nervous system (PNS) symptoms. We also examined heterogeneity of associations with estimated ambient styrene levels by race and sex. RESULTS: One-third of participants reported at least one neurologic symptom. The highest quartile of estimated ambient styrene was associated with one or more neurologic (PR, 1.12; 95% CI: 1.07,1.18), CNS (PR, 1.17; 95% CI: 1.11,1.25), and PNS (PR, 1.16; 95% CI: 1.09,1.25) symptom. Results were less consistent for biomarker analyses, but blood styrene level was suggestively associated with nausea (PR, 1.78; 95% CI: 1.04, 3.03). In stratified analyses, we observed the strongest effects among non-White participants. CONCLUSIONS: Increasing estimated ambient styrene concentration was consistently associated with increased prevalence of neurologic symptoms. Associations between blood styrene levels and some neurologic symptoms were suggestive. Environmental styrene exposure levels may be sufficient to elicit symptomatic neurotoxic effects.

Predictors of blood volatile organic compound levels in Gulf coast residents.

To address concerns among Gulf Coast residents about ongoing exposures to volatile organic compounds, including benzene, toluene, ethylbenzene, o-xylene, and m-xylene/p-xylene (BTEX), we characterized current blood levels and identified predictors of BTEX among Gulf state residents. We collected questionnaire data on recent exposures and measured blood BTEX levels in a convenience sample of 718 Gulf residents. Because BTEX is rapidly cleared from the body, blood levels represent recent exposures in the past 24 h. We compared participants' levels of blood BTEX to a nationally representative sample. Among nonsmokers we assessed predictors of blood BTEX levels using linear regression, and predicted the risk of elevated BTEX levels using modified Poisson regression. Blood BTEX levels in Gulf residents were similar to national levels. Among nonsmokers, sex and reporting recent smoky/chemical odors predicted blood BTEX. The change in log benzene was -0.26 (95% CI: -0.47, -0.04) and 0.72 (0.02, 1.42) for women and those who reported odors, respectively. Season, time spent away from home, and self-reported residential proximity to Superfund sites (within a half mile) were statistically associated with benzene only, however mean concentration was nearly an order of magnitude below that of cigarette smokers. Among these Gulf residents, smoking was the primary contributor to blood BTEX levels, but other factors were also relevant.