Environmental Styrene Research Articles

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 (). 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 ( log microns; 95% CI: , and log microns; 95% CI: , , 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

Environmental styrene exposure and sensory and motor function in gulf coast residents

Environmental styrene exposure and sensory and motor function in gulf coast residents

Determinants of environmental styrene exposure in Gulf coast residents

Determinants of environmental styrene exposure in Gulf coast residents

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

BackgroundStyrene 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. MethodsWe 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. ResultsOne-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. ConclusionsIncreasing 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.

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

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

Sensitivity maximization of leaky and weaky radiation micro/nano fiber sensors

The maximization of sensitivities of both leaky and weakly radiation micro/nano fiber sensors based on the refractive index occurred by choose the suitable core material (nf) for each environmental material (ne) with a specific wavelength (λmax) at which the highest sensitivity is achieved. Where the refractive indices nf and ne are wavelength dependent. For the leaky radiation microfiber sensor, the value of nf less than and getting close to the value of ne. The core material can be available with environmental material at some wavelengths and not suitable with other wavelengths. Such as, the core (BK7 glass) unsuitable with styrene within band rejected wavelengths (λ = 0.783–1.033) from the transmittance range of styrene (λ = 0.4386–1.052 μm). The radiation angle sensitivity (Sθ) becomes very high with wavelength (λSθmax) at which nf ≈ ne. Such as, core (BK7 glass) and environmental (styrene) at λmax = 0.8 μm, the value of Sθ = 13759. In the weakly radiation, the value of nf greater than the value of ne. The sensitivity is evaluated by measurement the mode field radius (SW) or the fiber core power (SP). For core (BK7) and environmental (toluene) with core radius a = 1 μm, the sensitivity Sw = 2556 (μm/RIU) at λ = 1.75 μm and the sensitivity SP = 22.3 Pi (power unit/RIU) at λ = 1.05 μm (Pi is the fiber input power). The numerical evaluation of leaky radiation angle (θ) and sensitivity (Sθ) are excellent if they are compared with the published experimental measured results. The leaky and weakly sensors has potential applications due to their high sensitivity and simple constructions.

Analysis of Styrene and its Metabolites in Blood and Urine of Workers Exposed to both Styrene and Acetone

A purge-and-trap gas chromatographic (PT-GC) method for determining styrene concentrations in urine and blood samples has been used in the biological monitoring of workers exposed to styrene and acetone. Blood and urine samples were collected from 34 individuals exposed to both solvents at the end of a 4-h shift and measured for styrene in urine (Su), blood (Sb), and the two major urinary metabolites, mandelic acid (MA) and phenylglyoxylic acid (PGA). A second urine sample was taken at the beginning of the next shift. Environmental exposure was measured using passive personal monitoring and GC. Urinary excretion of MA and PGA was measured by high-performance liquid chromatography. The average exposures to styrene and acetone were 70.5 mg/m3 and 370.5 mg/m3, respectively. In end-of-shift samples there was a significant correlation between concentrations of Su and Sb and the metabolites PGA, MA (r = 0.714 and 0.788, p < 0.001 for Su and r = 0.644 and 0.566, p < 0.005 for Sb). A high correlation between Sb and Su (r = 0.732, p < 0.001) also existed. Poor correlations were found between Su and metabolites in samples collected at the beginning of the next shift (r = 0.491 and 0.474 for PGA and MA, respectively, p < 0.05). There was a better correlation between the biological parameters at the end of the shift and the environmental styrene (r = 0.841 for PGA, r = 0.834 for MA, r = 0.788 for Su, and r = 0.698 for Sb; p < 0.001) compared with those at the start of the shift (r = 0.81 for PGA, 0.675 for MA, and 0.650 for Su; p < 0.001). We found that the concentration of excreted metabolites decreased significantly when environmental concentrations of acetone increased (p < 0.05), particularly at the end of the shift. Although the best correlation with environmental styrene was obtained with the sum of PGA and MA at the end of the shift (r = 0.862, p < 0.001), urine and blood styrene were shown to be more useful biological monitoring indicators because their concentrations were not affected by acetone co-exposure.

Urinary Excretion of Thioethers Related to Styrene Exposure

Urinary Excretion of Thioethers Related to Styrene Exposure: Ginette Truchon et al. Institut de recherche en santé et en sécurité du travail, Montréal, Québec, Canada—The objective of this study was to test the suitability of styrene‐specific mercapturic acids as urinary bioindicators of occupational styrene exposure. The excretion of mandelic acid (MA), global thioethers and styrene‐specific mercapturic acids was measured in urine samples from 64 workers employed in three companies fabricating glass fiber‐reinforced polyester products. Global thioethers were measured by a spectrophotometric method while MA and specific mercapturic acids, N‐acetyl‐S‐(1‐phenyl‐2‐hydroxyethyl)‐L‐cysteine (M1) and N‐acetyl‐S‐(2‐phenyl‐2‐hydroxyethyl)‐L‐cysteine (M2), were measured by high pressure liquid chromatography with UV detection. Excretion of M1 and M2 was qualitatively verified by gas chromatography‐mass spectrometry. The environmental measurements were carried out with passive dosimeters. Workers had 8‐h TWA exposure levels ranging from 0 to 667 mg/m3. End‐of‐shift MA excretion ranged from 0 to 2.08 mmol/mmol creatinine and was well correlated with environmental styrene exposure (r=0.91, p&lt;0.001). M1 and M2 were detected (i.e. above ca. 1 μmol/mmol creatinine) in urine samples of only three workers who were exposed to various concentrations of styrene. End‐of‐shift excretion of global thioethers was found to be significantly correlated to cigarette consumption as well as to styrene exposure, as measured by end‐of‐shift MA excretion. In opposition to data from rats, our results indicate that humans exposed to styrene excrete little styrene‐specific thioethers. The apparent inter‐individual variability in excretion of M1 and M2 suggests that they may not constitute suitable indicators of occupational styrene exposure.

Evaluation of styrene in air by thermal desorption-gas chromatography

A method to quantify the environmental styrene of occupationally exposed workers has been established. A diffusive sampler, that can be analysed by using thermal desorption-gas chromatography, was used to adsorb styrene from the ambient environment. A laboratory study was carried out to evaluate the performance of the sampler and to determine the styrene uptake rate, following the criteria adopted in European Standard 848. Finally, the proposed method has been checked under real conditions by evaluating styrene levels from an exposed population. There were no significant differences with the results obtained by other sampling methods.

Urinary excretion of specific mercapturic acids in workers exposed to styrene.

Styrene is an important chemical of wide industrial use, particularly in the manufacture of polymers and reinforced plastics. Environmental and occupational exposures to styrene occur predominantly via inhalation. Styrene undergoes biotransformation mainly by side chain oxidation catalyzed by cytochrome P-450 enzymes to its reactive metabolite, styrene oxide. The (R)- and (S)-enantiomers of styrene oxide can be conjugated with glutathione to both (R)- and (S)-diastereoisomers of specific mercapturic acids, N-acetyl-S-(1-phenyl-2-hydroxyethyl)-L-cysteine (M1) and N-acetyl-S-(2-phenyl-2-hydroxyethyl)-L-cysteine (M2). We conducted this biomonitoring study with the aim of evaluating the association between excretion of specific mercapturic acids (M1 and M2) and level of exposure to styrene among occupationally exposed people. The mean time-weighted average (TWA) exposure was about one-half the current threshold limit value, the range of the values varied from 44 to 228 mg/m3. Geometric mean (GM) concentrations of 650, 1,084, and 31.8 micrograms/g creatinine were measured, respectively, for M1-S, M2, and M1-R. The environmental styrene concentration exhibited a significant correlation with total specific mercapturic acid (Mtot = sum of M1-R, M1-S, and M2), making it possible for the first time to calculate the approximate relationship between styrene uptake and excretion of these substances. The M2 mercapturic acid had a better correlation (r = 0.56) with respect to M1-R and M1-S. Significant correlations were found also between the excretion of specific mercapturic acids and biological exposure indices (i.e., mandelic and phenylglyoxylic acids and urinary styrene).

Biological monitoring of exposure to low concentrations of styrene.

A field study was conducted on 39 male workers exposed to styrene at concentrations below 40 ppm (time weighted average, TWA). Analyses were carried out on environmental air, exhaled air, blood, urine, and two major urinary metabolites of styrene: mandelic acid (MA) and phenylglycoxylic acid (PGA). Head space gas chromatography (GC) with a flame ionization detector (FID) was used for determination of styrene in blood and urine. Postexposure exhaled air was analyzed using capillary GC. Environmental styrene exposure was measured by personal sampling using carbon cloth personal samplers. Urinary metabolites of styrene were determined by high pressure liquid chromatograph (HPLC). When the end-of-shift breath, blood, and urine styrene levels were compared with environmental TWA values, blood styrene correlated best with styrene in air (r = 0.87), followed by breath styrene (r = 0.76). Poor correlation (r = 0.24) was observed between environmental styrene exposure and urine styrene. When styrene metabolites were compared with environmental styrene, the sum of urinary MA and PGA correlated better with styrene in air than MA or PGA alone. The correlations between urinary metabolites and environmental styrene improved when corrected for the specific gravity of urine. Even better correlations were observed when the urinary metabolites were corrected for creatinine. The correlation coefficients for environmental styrene and end-of-shift MA, PGA, and MA+PGA were 0.83, 0.84, and 0.86, respectively. The correlation coefficients between environmental styrene and next morning urinary metabolites fell to 0.47, 0.61, and 0.65 for MA, PGA, and MA+PGA, respectively. These results suggest that determination of the total MA and PGA in urine samples is preferred than separate measurements of MA or PGA. The good correlation between environmental exposure and styrene in the exhaled air also suggests that breath styrene level can be a useful indicator for low level styrene exposure, as the method is specific, noninvasive, and rapid. Urinary styrene seems to be a less reliable indicator for low level styrene exposure.

Blood styrene concentrations in a "normal" population and in exposed workers 16 hours after the end of the workshift.

Blood styrene was measured by a gas chromatography-mass spectrometry method in 81 "normal people" and in 76 workers exposed to styrene. In the normal subjects, styrene was also tested in alveolar and environmental air. Styrene was found in nearly all (95%) blood samples. Average styrene levels in the normal subjects were 221 ng/l in blood (Cb), 3 ng/l in alveolar air (Ca) and 6 ng/l in environmental air (Ci). Styrene levels did not differ significantly between smokers and nonsmokers, 95% of values being below 512 ng/l in Cb, 7 ng/l in Ca and 15 ng/l in Ci. In workers with an average exposure to styrene of 204 micrograms/l, at the end of the workshift, mean blood styrene concentration was 1211 micrograms/l. In blood samples collected at the end of the Thursday shift, styrene levels were significantly higher (1590 micrograms/l) than those found at the end of the Monday shift (1068 micrograms/l). A similar difference was found in samples taken the morning after exposure (60 and 119 micrograms/l, respectively). Significant correlations between blood and environmental styrene were found both at the end of the shift and the morning after exposure (r = 0.61 and 0.41, respectively). In workers occupationally exposed to styrene, 16 h after the end of the workshift, blood styrene (94 micrograms/l) was significantly higher than that found in the normal subjects (0.22 microgram/l). The half-life of blood styrene was 3.9 h.

Urinary styrene in the biological monitoring of styrene exposure.

The urinary excretion of styrene represents a promising indicator of exposure to this solvent. Nevertheless extensive research under field conditions is scant. In this investigation 214 styrene-exposed workers from 10 fiberglass-reinforced plastics factories were studied. Environmental monitoring was performed by personal passive sampling. Blood styrene and the urinary excretion of styrene and its main metabolites, mandelic acid (MA) and phenylglyoxylic acid (PGA), were measured. The correlation coefficient between the time-weighted average of environmental styrene and the mean urinary excretion of styrene was 0.88 (0.91 after logarithmic transformation), compared with the 0.82 and 0.78 of the end-of-shift MA and PGA values, respectively. A high correlation (0.86) was also found between styrene in the blood and urine. The results, obtained under field conditions with a large group of exposed workers, confirm the usefulness of the urinary excretion of styrene as an exposure index for the biological monitoring of styrene exposure.

Determination of Mandelic Acid and Phenylglyoxylic Acid in the Urine and Its Use in Monitoring of Styrene Exposure

This paper describes a sensitive biological monitoring method for assessing exposure to styrene. Two major metabolites of styrene, mandelic acid (MA) and phenylglyoxylic acid (PGA), were measured in urine using reversed-phase high-performance liquid chromatography with a variable wavelength UV detector. The urine sample (200 microL) was saturated with 60 mg of sodium chloride and spiked with 20 microL of internal standard (O-methyl hippuric acid). Hydrochloric acid (6N HCl) was added for acidification followed by extraction with ethyl acetate. The extract (0.5 mL) was dried and reconstituted with the mobile phase. The mobile phase used was water-methanol (90:10) with 0.5% acetic acid. The filtrate (5 microL) was injected into the HPLC with a C18 column. The detection limits for MA and PGA were estimated to be 5 mg/L and 0.5 mg/L, respectively. The average recovery was 96% for MA and 84% for PGA. The between-days coefficients of variation for both metabolites were generally less than 11%. The average within-day variations were usually less than 5%. The method was verified with urine samples collected from workers exposed to styrene. Excellent correlations were observed between environmental styrene exposure and urinary MA (r = 0.92) and PGA (r = 0.85), determined by using the present method. The procedure is sensitive and reproducible, and can be applied to occupational health measurement of styrene exposure.

Chromosome aberrations and micronuclei in lymphocytes of workers exposed to low and medium levels of styrene.

In the present study we analysed 19 workers exposed to styrene in two factories where polyester resins were used. Because of the different sizes of the pieces undergoing resin processing, the environmental styrene concentrations and urinary mandelic acid (MA) levels of the analysed subjects were quite different in the two plants examined. Cytogenetic monitoring was performed by analysis of chromosome aberrations (CAs) and micronuclei (Mn) in peripheral blood lymphocytes. Cytogenetic analysis revealed a significant increase in the percentage of aberrant cells and total aberrations in the group with higher styrene exposure (group 2) and no increase in the group with lower exposure (group 1), as compared with matched controls. Mn frequencies were not significantly increased in the two exposed populations. No correlations between length of exposure and CA or Mn frequency were found, and a weak correlation was found between exposure levels, measured as urinary MA, and Mn frequencies. Only 5 of the 12 exposed workers examined in group 2 had urinary MA levels higher than the limit recommended by the ACGIH in 1990-91 [1]. Significant increases in DNA damage are therefore already found at urinary MA levels lower than the internationally suggested exposure limits.