Behavioral alterations due to diesel exhaust exposure

Several experiments examining the effects of diesel exhaust on the behavior of rats are reported. Animals were exposed either as adults or neonates. The spontaneous locomotor activity (SLA), measured in standard running wheel cages, of adult rats exposed for 8 h/day, 7 days/week was significantly less than that of controls. Experiments involving diesel exhaust exposure to neonatal rats indicated that adult rats, exposed to diesel exhaust during their neonatal lives, were significantly less active as measured by SLA. Adult rats, exposed to 20 h diesel per day as neonates, were placed in skinner boxes after the SLA experiment described above had been completed. The exhaust exposed animals showed significantly decreased acquisition of a food reinforced bar pressing task. All animals that learned this task extinguished at the same rate. The results of the neonatal diesel exhaust experiments support the hypothesis that diesel exhaust exposure during development of an organism can lead to behavioral differences in adulthood.     

Never smoker lung cancer risks from exposure to particulate tobacco smoke

The average particulate environmental tobacco smoke (ETS) exposure of never and current smokers and the average lung cancer mortality rate for current smokers is estimated from empirical data. These estimates are used in a linear downward extrapolation of the lung cancer risk/mg of particulate ETS exposure for current smokers to calculate the average lung cancer risk for never smokers and the number of never smoker lung cancer deaths (LCD) in the U.S. in 1980 from exposure to particulate ETS. The estimated average daily inhaled particulate ETS exposure for never smokers is 0.62 mg/day for men and 0.28 mg/day for women. The average never smoker is estimated to retain 11% of the inhaled exposure, for a daily retained exposure of 0.07 mg for men and 0.03 mg for women. Other estimates are: a daily retained exposure for current smokers of 310 mg for men and 249 mg for women, a smoking-attributable lung cancer risk for current smokers in 1980 of 284 LCD/100,000 men and 121 LCD/100,000 women, and an annual retained-exposure lung cancer risk for never smokers of 0.64 LCD/100,000 men and 0.015 LCD/100,000 women. These risks and exposures estimate 12 lung cancer deaths among never smokers from exposure to particulate ETS: 8 among the 11.96 million male never smokers and 4 among the 28.85 million female never smokers in the U.S. in 1980. Conversely, between 655 and 3,610 never smoker lung cancer deaths are estimated from methods based on the average lung cancer risk observed in epidemiological studies of exposure to ETS. Three possible reasons for the discrepancy between the exposure and risk-based estimates are discussed: the excess risks observed in epidemiological studies are due to bias, the relationship between exposure and risk is supralinear, or sidestream tobacco smoke is substantially more carcinogenic than an equivalent exposure to mainstream smoke.     

Pesticide exposure and lung cancer mortality in Leningrad province in Russia

This study was carried out to examine the association between pesticide exposure and lung cancer mortality. We conducted an autopsy based case-control study in Leningrad Province in Russia. A total of 540 lung cancer cases and 582 controls were identified among subjects who had died in the hospitals of the Leningrad province between 1993 and 1998. Using work history records, we assessed exposure to pesticide at the level of industry and job title. Unconditional logistic regression was used to calculate adjusted odds ratio for pesticide exposure and lung cancer mortality. There was no association between ever exposure to pesticide and lung cancer mortality overall (odds ratio=1.06, 95% confidence interval=0.82-1.36) and in both men (odds ratio=1.11, 95% confidence interval=0.84-1.46) and women (odds ratio=0.74, 95% confidence interval=0.37-1.46). We observed no statistically significant odds ratio by duration of pesticide exposure, intensity of pesticide exposure, and cumulative pesticide exposures with lung cancer mortality in both smokers and nonsmokers. Odds ratio also did not differ when the analysis was restricted to individuals who had exposure data with high confidence scores. Our findings suggest no associations between pesticide exposures and mortality of lung cancer in the population of the Leningrad province in Russia that deserves further evaluation.     

Physical characterization of diesel exhaust particles in exposure chambers

Since the deposition of particulate in the respiratory system is strongly influenced by particle size, a correct assessment of this parameter is important for any inhalation experiment studying the potential health effects of air pollutants. Measuring the distribution of particles according to their aerodynamic diameter and mechanical mobility diameter is crucial in analyzing the deposition of submicron particles in the lower respiratory system. Cascade impactor measurements of diluted diesel exhaust in 12.6 m³ animal exposure chambers in the GMR Biomedical Science Department showed that the mass median aerodynamic diameter of the aerosol was 0.2 μm with 88% of the mass in particles smaller than 1 μm. Diffusion battery measurements showed that the mass median mechanical mobility diameter was about 0.11 μm. Transmission electron micrographs of particles deposited on chamber surfaces revealed both agglomerates and nearly spherical particles. The particles in these chambers are similar in size and shape to diesel particles described elsewhere. The flux of diesel particles to food surfaces was measured. Calculations of the expected daily dose by inhalation and by feeding showed that the “worst case” dose by feeding was only about one-tenth the dose by breathing.     

Enhanced susceptibility to infection in mice after exposure to dilute exhaust from light duty diesel engines

A series of experiments was conducted in which groups of mice were first exposed for various durations to diluted exhaust from light duty diesel engines and then briefly to an infectious aerosol generated by nebulizing cultures of a bacterial pathogen (Streptococcus). Typically, postinfection mortality was significantly greater in groups exposed to exhaust than in their corresponding control groups exposed to purified air only. Data of recent diesel and of past diesel- and catalyst-treated gasoline engine exhaust experiments suggest a somewhat greater excess mortality from (enhanced susceptibility to) bacterial infection in mice exposed to diesel exhaust than in those exposed to catalytic gasoline exhaust. Limited data on acute tests of NO₂ and acrolein vapor alone suggest that the infectivity-enhancing effect of diesel exhaust could be accounted for in large part by these components. Exposures to diesel exhaust, NO₂, or acrolein did not enhance the mortality response to a viral pathogen (A/PR8-34).     

An industrial hygiene characterization of exposure to diesel emissions in an underground coal mine

Problems exist in the United States' effort to achieve energy self-sufficiency. Increasing coal production to assure energy self-sufficiency is a prime problem for the rest of the century and beyond. The use of diesels in underground coal mines has been suggested as a mining method to aid in this needed, increased production. Many questions exist about the effects on humans in such environments. NIOSH Division of Respiratory Disease Studies has undertaken a research effort to characterize the environments of existing diesel coal mines. The results of one of the studies will be presented. Preliminary assessments of carbon monoxide, nitrogen dioxide, C₁-C₅ aldehydes and organic acids, aliphatic hydrocarbons, sulfates, total and respirable dust, and polycyclic aromatic hydrocarbons (PAH) are presented. Nitrogen dioxide and total aldehydes are suggested as possible species to quantify diesel exposure.     

Pulmonary function evaluation of cats after one year of exposure to diesel exhaust

Adult male, inbred, disease-free cats of uniform age and size were exposed eight hours per day, seven days per week to a 1 : 18 dilution of diesel exhaust emissions. After one year of exposure, the animals were removed from the chambers for measurement of lung volumes, forced expiratory flow rates, dynamic compliance and resistance, diffusing capacity, and nitrogen washout. No important changes in pulmonary function were detected with the exception of a decrease in closing volume (P < 0.05). The inability to detect decrements in pulmonary function may have been due to insufficient cocentration of exhaust, insufficient exposure length, or to the use of a species resistant to diesel exhaust. To test these possibilities, the cats are being exposed for an additional year, and another species, hamsters, are being exposed for future testing at exhaust dilutions of 1 : 18 and 1 : 9.     

Neurophysiological alterations due to diesel exhaust exposure during the neonatal life of the rat

This study was designed to assess the effects of diesel exhaust on the development of the nervous system in rats as measured by somatosensory and visual evoked potentials (SEPs and VEPs, respectively). SEPs, elicited by 1 mamp, 0.5 msec pulses delivered to the tibial nerve at the tibale, were recorded from the skull overlying the somatosensory projection area on days 28, 35, 42, and 49 postconception (pc). Analysis of the data for day 35 pc double pulse SEPs revealed significantly longer latencies for all peaks of the SEP in pups exposed to diesel exhaust. There were also differences indicating that the electrophysiological recoverability of the nervous system had been compromised in the diesel exhaust exposed group. On day 35 pc, the latencies of all VEP peaks occurring before 300 msec were greater in the exposed group. The differences, however, reached statistical significance only for the P2 peak of the response to the first of the paired stimuli. These data support the hypothesis that diesel exhaust influences the development of the nervous system.     

Behavioral difficulties in 7-year old children in relation to developmental exposure to perfluorinated alkyl substances

BackgroundPerfluorinated alkyl substances (PFAS) are suspected endocrine disruptors that are highly persistent and neurotoxic in animals. Human epidemiological studies of exposure-related deviations of children's behaviors are sparse. We assessed the associations between prenatal, 5- and 7-year PFAS exposures and behavioral problem scores in 7-year Faroese children.MethodsConcentrations of perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorodecanoic acid (PFDA), perfluorooctane sulfonate (PFOS), and perfluorohexane sulfonic acid (PFHxS) were measured in maternal serum and in serum from children at ages 5 and 7 years (n = 539, 508, and 491, respectively). We used multivariable regressions and structural equations models to estimate the covariate-adjusted associations between serum-PFAS concentrations and behavioral difficulties, as assessed by the strengths and difficulties questionnaire (SDQ) at age 7.ResultsSerum-PFOS and PFHxS concentrations declined over time, whereas PFOA, PFNA, and PFDA tended to increase. No associations were observed between prenatal PFAS concentrations and SDQ scores. However, a two-fold increase in 5-year serum-PFOA, PFNA, and PFDA concentrations was associated with increases in total SDQ scores by 1.03 (95% CI: 0.11, 1.95), 0.72 (95% CI: 0.07, 1.38) and 0.78 points (95% CI: 0.01, 1.55), respectively. For SDQ subscales, significant associations were found in regard to hyperactivity, peer relationship, and conduct problems, as well as internalizing and externalizing problems and autism screening composite scores. Cross-sectional analyses at age 7 years showed possible sex-dimorphic associations between PFAS concentrations and SDQ scores, where girls had consistently positive associations with SDQ scores whereas boys exhibited a pattern of negative or null associations.ConclusionsHigher serum PFAS concentrations at ages 5- and 7-years, but not prenatally, were associated with parent-reported behavioral problems at age 7.     

Indoor air exposure to coal and wood combustion emissions associated with a high lung cancer rate in Xuan Wei, China

Residents of Xuan Wei County in China have unusually high lung cancer mortality that cannot be attributed to tobacco use or occupational exposure. They are exposed to smoke from unvented, open pit coal or wood fires (often used for cooking and heating). The variation in lung cancer rates among communes within the county suggests that indoor combustion of smoky coal may be the prime determinant of lung cancer. To characterize the air in Xuan Wei homes, samples of air particles and semivolatile organic compounds were collected from homes located in two communes; one commune has a high rate of lung cancer, and the other has a low rate. Samples collected in the commune where the lung cancer rate is high and where smoky coal is the predominant fuel contained high concentrations of small particles with high organic content; organic extracts of these samples were mutagenic. Samples from homes in the wood-burning commune, which has a low rate of lung cancer, consisted mostly of larger particles of lower organic content and mutagenicity. The smoky coal sample was a mouse skin carcinogen and was a more potent initiator of skin tumors in comparison to the wood or smokeless coal sample.     

Maternal exposure to high levels of dioxins in relation to birth weight in women affected by Yusho disease

Background

Studies on the association of maternal exposure to polychlorinated dibenzo-p-dioxin (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) with decreased birth weight in humans have produced conflicting results. In Japan in 1968, an accidental human exposure to rice oil contaminated with PCDDs, PCDFs, and PCBs, led to the development of Yusho disease.

Objective

The Yusho cohort was used to evaluate the effect of maternal exposure to PCDDs, PCDFs, and PCBs on birth weight.

Methods

Blood samples, obtained from 101 Yusho women (190 births) who gave birth after exposure, were analyzed for congeners of seven PCDDs, ten PCDFs, and four non-ortho PCBs.

Results

Total PCDD TEQ (adjusted beta = − 161.9 g; 95% CI, −265.3 to − 58.6), total PCDF TEQ (adjusted beta = − 105.9 g; 95% CI, −179.5 to − 32.2), and total non-ortho PCBs (adjusted beta = − 178.4 g; 95% CI, −318.3 to − 38.5) levels were inversely associated with birth weight. Significant inverse associations with birth weight were also found for total PCDD TEQ, total PCDF TEQ, and total non-ortho PCB TEQ levels among male, but not female, infants. Significant inverse associations with birth weight were also found for nine congeners among all infants; the adjusted beta coefficients were largest for 1,2,3,6,7,8-HxCDD and smallest for 2,3,4,7,8-PeCDF.

Conclusion

In the setting of exposure to high levels of dioxins, maternal blood levels of PCDDs, PCDFs and PCBs are associated with lower birth weight in Yusho patients. The association exhibited gender-specific differences, as male infants are more susceptible than females to growth restriction induced by in utero dioxin exposures.     

Inorganic arsenic exposure and its relation to metabolic syndrome in an industrial area of Taiwan

Past arsenic exposure was found associated with increased incidence of type 2 diabetes. However, the mechanisms remain unclear. Metabolic syndrome has been shown as a strong predictor for diabetes occurrence. We aimed at examining the association of inorganic arsenic exposure and the prevalence of metabolic syndrome. The authors recruited 660 age and gender stratified random population of residents in central Taiwan during 2002-2003. They received home interviews and health examinations at local health care units, where blood and hair specimens were collected. Hair arsenic (H-As) concentrations were determined by inductively coupled plasma-mass spectrometry. Metabolic syndrome was defined as the presence of three or more of the following risk factors: elevated levels of blood pressure, plasma glucose, and triglycerides, also the body mass index, and reduced high-density lipoprotein. Prevalence of metabolic syndrome increased from the 2nd tertile (0.034 ug/g) of H-As levels (odds ratio=2.54, 95% confidence interval: 1.20-5.39, p=0.015) after the adjustment for age, gender, occupation and life styles including cigarette smoking. We further found linear relation between H-As concentrations and increased levels of plasma glucose and lipids, and blood pressures. This first report may help identify modifiable factors associated with diabetogenesis and cardiovascular disease progression and thus be worth following for community health.     

Breast cancer incidence and exposure to pesticides among women originating from Jaipur

Environmental contamination by pesticides has been documented in biotic and abiotic components. These persistent organic pollutants are lipid soluble, nonbiodegradable, and endocrine disrupters. The present study was therefore planned to determine whether the levels of these pesticides like DDT and its metabolites DDD and DDE, dieldrin, heptachlor, and HCH and its isomers (alpha, beta, and gamma) were higher in blood of breast cancer patients when compared with normal women who did not suffer from major diseases like blood pressure, tuberculosis, diabetes, thyroid dysfunction, arthritis, cancer, etc. and had not undergone any major surgery. The results indicated that organochlorine pesticides taken for analysis were found significantly high in breast cancer patients irrespective of age, diet, and geographic distribution.     

Lymphatic transport of inhaled diesel particles in the lungs of rats and guinea pigs exposed to diluted diesel exhaust

Factors influencing the disposition of the inhaled diesel particles were studied by analyzing the deposition of radioactively labelled diesel particles in the respiratory system, by determining the specific function of alveolar cellular mechanisms in the primary defense against inhaled particles and by identifying the important role of the lymphatic system in the lung clearance of experimental animals exposed to diluted emissions from a diesel engine. Radioactive ¹³¹Barium was used as a tracer of diesel particles and the deposition efficiency was determined to be 15%±6% of the inhaled dose in the Fischer 344 rat strain. The number of cells obtained by bronchial lavage increased significantly after a prolonged exposure to a concentration of 1500 μg/m³ of diesel particles. The increased cell number was more than twofold, contained two distinct cell populations (alveolar macrophages and neutrophils) and represented a reactive mobilization of the defense mechanisms in the organism. Light microscopy studies investigated the role of lymphatic transport of the particulate matter and revealed that the peribrochial and perivascular aggregates of lymphoid tissue contained diesel particles even after short exposure periods at low dose levels. With the increasing burden of particles in the respiratory system, the coloration of hilar and mediastinal lymph nodes continuously changed to gray and finally to dark black, depending upon the dose level and exposure. However, at all exposure levels, most of the diesel particles in the alveoli were phagocytized by an increased alveolar cellular defence and particle-containing macrophages were actively moving towards the mucociliary escalator or towards lymphatic channels leading to peribronchial lymphoid aggregates and bronchial or mediastinal lymph nodes. In the lymph nodes, alveolar macrophages containing diesel particles were found mostly in the afferent subcapsular lymphatic vessels and marginal sinuses. In the later stages, cellular structure disintegrated and large aggregates of particulate matter were dispersed throughout the medullary cords with increasing accumulation towards the hilus. It is concluded that the lymphoid aggregates and lymphatic nodes play an important role in sequestering diesel particles or particle-containing phagocytizing cells and provide a pathway, in addition to the mocociliary clearance for particulate removal from the deep pulmonary region.     

Dietary exposure to cadmium and risk of breast cancer in postmenopausal women: A systematic review and meta-analysis

BackgroundWith tobacco smoking, diet is the main source of cadmium (Cd) exposure in the general population. The carcinogenic and estrogenic activities of Cd make it a contaminant of potential concern for hormone-dependent cancers including breast cancer. Postmenopausal women represent the most appropriate population to investigate the possible impact of exogenous factors with potential estrogenic activity on breast cancer as, after menopause, their estrogenic influence is predominant.ObjectivesWe systematically reviewed available studies on the association between dietary exposure to Cd and breast cancer focusing on postmenopausal women. A meta-analysis combining the risk estimators was performed and potential sources of between studies heterogeneity were traced.MethodsStudies were searched from MEDLINE through 31 January 2015 and from the reference lists of relevant publications. Six eligible studies published between 2012 and 2014 were identified and relative risk estimates were extracted. Meta-rate ratio estimates (mRR) were calculated according to fixed and random-effect models. Meta-analyses were performed on the whole set of data and separate analyses were conducted after stratification for study design, geographic location, use of hormone replacement therapy (HRT), tumor estrogen receptor status (ER + or ER −), progesterone receptor status (PGR + or PGR −), body mass index (BMI), smoker status, zinc or iron intake.ResultsNo statistically significant increased risk of breast cancer was observed when all studies were combined (mRR = 1.03; 95% confidence interval [CI]: 0.89–1.19). Several sources of heterogeneity and inconsistency were identified, including smoker status, HRT use, BMI, zinc and iron intake. Inconsistency was also strongly reduced when only considering ER −, PGR −, tumors subgroups from USA and from Japan. The risks were, however, not substantially modified after stratifications. No evidence of publication bias was found.ConclusionThe present study does not provide support for the hypothesis that dietary exposure to Cd increases the risk of breast cancer in postmenopausal women. Misclassification in dietary Cd assessment in primary studies could have biased the results towards a finding of no association.     

Lactational exposure to phthalates in Southern Italy

BackgroundPhthalates, reproductive toxicants in animals, are synthetic chemicals with ubiquitous human exposures because of their extensive use, with potential detrimental health effects. Infants are considered to represent a population at increased risk, as they are exposed early in life to several different sources of exposure to phthalates.Objectives and methodsLittle information exists on phthalate exposure through breast milk from different geographic areas. By means of a LC/LC–MS/MS method we tested the presence of several different phthalate metabolites in breast milk from 62 healthy mothers living in Southern Italy.ResultsThe simple monoesters mono-isobutyl phthalate (MiBP) (median 18.8 μg/l) and mono(2-ethylhexyl) phthalate (MEHP) (median 8.4 μg/l) were present in all milk samples, whereas mono-n-butyl phthalate (MnBP) (median 1.5 μg/l) and mono-benzyl phthalate (MBzP) (median < 0.3 μg/l) were found in 64.5% and 43.5% of the samples, respectively. Among the oxidative metabolites of DEHP and DiNP only mono(2-ethyl-5-carboxypentyl) phthalate (5cx-MEPP) and monoisononyl phthalate with one hydroxyl group (OH-MiNP) were detectable in one and 13 samples (21%), respectively.ConclusionsThese findings indicate that exposure to phthalates through breast milk in Southern Italian infants is comparable to that of other countries, thus confirming that human milk may represent an additional potential source of phthalate exposure in a population at increased risk. However, different milk concentrations of MiBP may suggest a different pattern of usage of di-iso-butyl phthalate in Europe, as compared to USA, whereas for the first time, we detected an oxidative DiNP metabolite, whose significance remains unclear.