Please cite this article as: Geng, X., Shao, H., Zhang, Z., Ng, J.C., Peng, C.,Malathioninduced testicular toxicity is associated with spermatogenic apoptosis and alterations in testicular enzymes and hormone levels in male Wistar rats, Environmental Toxicology and Pharmacology (2015), http://dx.doi.org/10. 1016/j.etap.2015.01.010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Malathion caused the reduction in the sperm counts and motility. The reduced body and testis weights were coupled with mild to severe degenerative changes in seminiferous tubules. We Page 3 of 32 A c c e p t e d M a n u s c r i p t 3 found malathion at 54 mg/kg increased spermatogenic apoptosis rate which was confirmed by changes in protein expression of Bax and Bcl-2. The activities of testicular enzymes including ACP, LDH and γ-GT were significantly altered with the reduced level of reproductive hormones such LH, FSH and T. These results indicate that malathion can elicit deleterious effects on reproductive system of rats. The abnormal levels of hormones and apoptotic proteins induced by malthion may play important roles.

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This study assesses the effects of long-term exposure to ambient air pollutants on inflammatory response and lung function. We selected 390 male coke oven workers with exposure to polycyclic aromatic hydrocarbons (PAHs) and fine particulate matter (PM) and 115 control workers. The average duration in the exposed group was 9.10 years. The total amount of PAHs was more enriched in PM which collected from the coke oven workshops compared with the control areas. Correspondingly, the internal PAHs exposure indicated by urinary 1-hydroxypyrene (1-OHP) in the exposure group increased 25.7-fold compared to that of the control group. Moreover, the increasing level of urinary 1-OHP was associated with the decrease of forced expiratory volume in 1 s to forced vital capacity ratio (FEV/FVC). In non-current smokers of exposure group, inverse correlation of 1-OHP with FEV/FVC was also found. Particularly, an exposure duration-dependent decline in FEV/FVC and mean forced expiratory flow between 25% and 75% of forced vital capacity (FEF) indicated that small airways were functionally obstructed. Furthermore, the increasing serum high-sensitivity C-reactive protein (hs-CRP) was correlated with the decline in pulmonary function in all subjects. These findings provide a clue that long-term exposure to PAHs-enriched PM impairs pulmonary function in occupational population.

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