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Objective: Evaluate whether childhood cancer incidence is associated with counties with hydraulic fracturing (HF). Methods: We compared cancer incidence in children in Pennsylvania counties before and after HF drilling began, using standardized incidence ratios (SIRs) and 95% confidence intervals (CIs). Results: The total number of cancers observed was close to expected both before drilling began (SIR = 0.94; 95% CI, 0.90 to 0.99) and after drilling (SIR = 1.02; 95% CI, 0.98 to 1.07) for counties with oil and natural gas wells. Analyses for childhood leukemia were also unremarkable (SIR for leukemia before drilling = 0.97 [95% CI, 0.88 to 1.06]; SIR for leukemia after drilling = 1.01 [95% CI, 0.92 to 1.11]). A slightly elevated SIR was found for central nervous system tumors after drilling (SIR = 1.13; 95% CI, 1.02 to 1.25). This was because of a slight excess in those counties with the fewest number of wells. Conclusions: This study offers comfort concerning health effects of HF on childhood cancers.

Questions persist about adverse effects such as impaired cognition and attention, incoordination, spasticity, or parkinsonism from chronic, low-level exposures to organophosphate (OP) compounds. In a prospective cohort study, we evaluated chlorpyrifos-manufacturing workers and a referent group on 2 occasions, 1 year apart, to determine whether occupational exposure to chlorpyrifos produced clinically evident central nervous system (CNS) dysfunction. Chlorpyrifos subjects had significantly higher TCP excretion and lower average BuChE activity than referents in a range in which physiological effects on B-esterases exist. Few subjects had neurologic symptoms or signs, and there were no significant group differences in terms of signs at baseline or second examinations. Chronic chlorpyrifos exposure produced no clinical evidence of cortical, pyramidal tract, extrapyramidal, or other CNS dysfunction among chlorpyrifos subjects compared with referents, either at baseline or after 1 year of additional chlorpyrifos exposure.

Background The ubiquitous dichlorodiphenyltrichloroethane (DDT) metabolite 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) is an androgen receptor antagonist. Data on potential antiandrogenic activity of DDE in humans are limited. Methods The relations between concentrations of plasma DDE and several serum androgens (total testosterone, bioavailable testosterone, 5alpha-dihydrotestosterone, and free androgen index) were examined in 137 North Carolina black male farmers, using multiple linear regression. Results Participants ranged in age from 30 to 88 years (mean = 62 years). Most had farmed for about 30 years and 27% reported having used DDT. The median DDE level was 7.7 microg per liter (1213 microg per kg lipid), slightly higher than in other recent studies. Overall, concentrations of DDE and androgens were unrelated. Total testosterone decreased 2% (95% confidence limits [CL] = -9%, 5%) per increase in interquartile distance of lipid-adjusted DDE. The percentage change in other hormones was similarly negligible. However, among those whose DDE level was in the top tenth percentile, compared with all others, total testosterone and free androgen index were lower by 23% (CL= -40%, 1%) and 22% (CL =-41%, 4%) respectively. Plasma androgen levels decreased with age, a relation that has previously been studied only in whites. Conclusions Studies of more highly exposed populations may be needed to evaluate effects, if any, of DDE.

We reviewed blink reflexes recorded from 51 railroad workers with long-term occupational exposure to solvents who were diagnosed by others with solvent-induced toxic encephalopathy. No worker fulfilled conventional clinical criteria for dementia or trigeminal mononeuropathy. All workers had normal R1 and R2 blink reflex latencies. Rl latencies correlated significantly with several nerve conduction measures, including F wave latencies, suggesting that some intersubject variability reflected intrinsic conduction properties, not isolated brain-stem function. Although normal, the workers' R1 latencies were significantly prolonged compared with historical control groups, including gender-matched control subjects of similar mean age (11.2 ms vs 9.9 ms; P < 0.0001). Stepwise multiple regression models demonstrated significant associations of R1 latency with age and use of CNS-active prescription medications (P = 0.003), but duration of occupational solvent exposure did not enter into the models. Paradoxically, workers using CNS-active medications had significantly shorter R1 latencies compared with workers not using such medications (10. 9 vs 11. 7 ms; P = 0.01). Job title, another potential surrogate measure of exposure, was not significantly related to reflex latencies. The geographical site of predominant solvent exposure did influence R1 latency, and workers from one site had longer exposure duration and longer R1 latencies than remaining workers. However, an interaction between age and exposure duration (r = 0.39; P = 0.003) confounded interpretation of this observation. Disability or work status, mental status findings, or classification of encephalopathy did not influence blink reflex latencies. The overall results do not support, but do not entirely exclude, a possible relationship between subclinical blink reflex abnormalities and occupational exposure to solvents. Nevertheless, it is clear from these results that the small group differences in R1 latency between exposed workers and control subjects are of no diagnostic importance and of uncertain physiologic importance, and they may reflect unrecognized confounders and technical factors.

Boron oxide has been shown in animals to irritate the respiratory mucosa and conjunctiva. The present study was undertaken to determine whether exposures to boron oxide and its hydration product, boric acid, cause respiratory and eye irritation in humans. One hundred thirteen workers exposed to these materials and 214 unexposed workers were interviewed regarding symptoms. Statistically significant associations were found between eye irritation, dryness of the mouth, nose, or throat, sore throat, and productive cough and mean exposures of 4.1 mg/m3 (which probably did not exceed 8.5 mg/m3).