Neonicotinoid insecticides that have been on the market since 1992 have been used globally including in Japan. Because they are sprayed over forests and agricultural areas, inadvertent toxicity in nontarget insects (especially honey bees) and humans is a matter of public concern. However, information on exposure levels and potential health impacts of neonicotinoids in children living around sprayed areas is scarce. Thus, we determined neonicotinoid exposure levels in children living in communities where thiacloprid was used to control pine wilt disease. A total of 46 children (23 males and 23 females) were recruited for the present study, and informed written consent was obtained from their guardians. Urine specimens were collected before, during, and after insecticide spraying events; and atmospheric particulate matter was also collected. Concentrations of thiacloprid and 6 other neonicotinoid compounds were determined in urine samples and in atmospheric particulate matter specimens using liquid chromatography‐electrospray ionization‐tandem mass spectrometry. In urine specimens, thiacloprid concentrations were <0.13 μg/L and were detectable in approximately 30% of all samples. Concentrations of the other neonicotinoids, N‐dm‐acetamiprid, thiamethoxam, dinotefuran, and clothianidin, were 18.7, 1.92, 72.3, and 6.02 µg/L, respectively. Estimated daily intakes of these neonicotinoids were then calculated from urinary levels; although the estimated daily intakes of the neonicotinoids were lower than current acceptable daily intake values, the children were found to be exposed to multiple neonicotinoids on a daily basis. Environ Toxicol Chem 2019;38:71–79. © 2018 SETAC
Studies of polycyclic aromatic hydrocarbons (PAHs) and its metabolites in PM10, soils, rat livers and cattle urine in Kumasi, Ghana, revealed high concentrations and cancer potency. In addition, WHO and IARC have reported an increase in cancer incidence and respiratory diseases in Ghana. Human urine were therefore collected from urban and control sites to: assess the health effects associated with PAHs exposure using malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OHdG); identify any association between OH-PAHs, MDA, 8-OHdG with age and sex; and determine the relationship between PAHs exposure and occurrence of respiratory diseases. From the results, urinary concentrations of the sum of OH-PAHs (∑OHPAHs) were significantly higher from urban sites compared to the control site. Geometric mean concentrations adjusted by specific gravity, GM, indicated 2-OHNaphthalene (2-OHNap) (6.01 ± 4.21 ng/mL) as the most abundant OH-PAH, and exposure could be through the use of naphthalene-containing-mothballs in drinking water purification, insect repellent, freshener in clothes and/or "treatment of various ailments". The study revealed that exposure to naphthalene significantly increases the occurrence of persistent cough (OR = 2.68, CI: 1.43-5.05), persistent headache (OR = 1.82, CI: 1.02-3.26), tachycardia (OR = 3.36, CI: 1.39-8.10) and dyspnea (OR = 3.07, CI: 1.27-7.43) in Kumasi residents. Highest level of urinary 2-OHNap (224 ng/mL) was detected in a female, who reported symptoms of persistent cough, headache, tachycardia, nasal congestion and inflammation, all of which are symptoms of naphthalene exposure according to USEPA. The ∑OHPAHs, 2-OHNap, 2-3-OHFluorenes, and -OHPhenanthrenes showed a significantly positive correlation with MDA and 4-OHPhenanthrene with 8-OHdG, indicating possible lipid peroxidation/cell damage or degenerative disease in some participants. MDA and 8-OHdG were highest in age group 21-60. The present study showed a significant sex difference with higher levels of urinary OH-PAHs in females than males.
Neonicotinoid insecticides (NNIs) are now popular in many agricultural systems across Africa; however, the extent of human exposures to NNIs in African countries is scarcely reported. The present study evaluates neonicotinoid exposures in the consumer population of Kumasi, a cosmopolitan city in Ghana. A total of 75 human urine samples were collected from healthy volunteers (nonfarmers, aged 13-80 yr) and analyzed with a liquid chromatography electrospray ionization tandem mass spectrometry system. Seven NNIs and 3 NNI metabolites were detected in the following pattern (frequency, median concentration, maximum concentration): N-dm-acetamiprid (94.7%, 0.41 µg/L, 8.79 µg/L) > imidacloprid (70.7%, 0.15 µg/L, 211.62 µg/L) > N-(6-chloro-3-pyridylmethyl)-N-ethyl-N′-methylformamidine (62.2%, 0.43 µg/L, 53.85 µg/L) > 2-[N-(6-chloro-3pyridylmethyl)-N-ethylamino]-2-(methylimino)acetic acid (56.8%, 0.10 µg/L, 3.53 µg/L) > clothianidin (40%, >limit of quantification [LOQ], 0.45 µg/L) > nitenpyram (18.7%, >LOQ, 0.14 µg/L) ≈ thiamethoxam (18.7%, >LOQ, 0.21 µg/L) > dinotefuran (12.0%, >LOQ, 1.01 µg/L) > acetamiprid (2.7%, >LOQ, 0.08 µg/L) ≈ thiacloprid (2.7%, >LOQ, 0.14 µg/L). Approximately 92% of the subjects were found to be exposed to multiple neonicotinoids simultaneously. The mean, median, and maximum imidacloprid equivalent of the relative potency factor of NNIs were found to be 1.6, 0.5, and 22.52, respectively. The median estimated daily intakes of acetamiprid, imidacloprid, and nitenpyram were 0.47, 1.27, and 0.02 µg/kg/d for females and 0.91, 0.66, and 0.08 µg/kg/d for males, respectively. The maximum daily intakes of all the NNIs were <1% of their chronic reference doses (cRfDs), except for imidacloprid and thiacloprid which recorded maximum daily intakes corresponding to 17.97 and 8.28% of cRfDs, respectively. To the best of our knowledge, the present study is the first biomonitoring report on neonicotinoid insecticides in Africa.
Toxicological effects of neonicotinoid insecticides (NNIs) have been reported for mammals, such as humans, rats, and mice. However, there are limited reports on their toxic effects on wild mammals. To predict NNI‐induced toxic effects on wild mammals, it is necessary to determine the exposure levels and metabolic ability of these species. We considered that raccoons could be an animal model for evaluating NNI‐induced toxicities on wildlife because they live near agricultural fields and eat crops treated with NNIs. The objective of the present study was to estimate the effects of NNI exposure on wild raccoons. Urinary concentrations of NNI compounds (n = 59) and cytochrome P450‐dependent metabolism of NNIs (n = 3) were evaluated in wild raccoons captured in Hokkaido, Japan, in 2020. We detected either one of the six NNIs or one metabolite, including acetamiprid, imidacloprid, clothianidin, dinotefuran, thiacloprid, thiamethoxam, and desmethyl‐acetamiprid in 90% of raccoons (53/59); the average cumulative concentration of the seven NNI compounds was 3.1 ng/ml. The urinary concentrations were not much different from those reported previously for humans. Furthermore, we performed an in vitro assessment of the ability of raccoons to metabolize NNIs using hepatic microsomes. The amounts of NNI metabolites were measured using liquid chromatography–electrospray ionization–tandem mass spectrometry and compared with those in rats. Raccoons showed much lower metabolic ability; the maximum velocity/Michaelis–Menten constant (Vmax/Km) values for raccoons were one‐tenth to one‐third of those for rats. For the first time, we show that wild raccoons could be frequently exposed to NNIs in the environment, and that the cytochrome P450‐dependent metabolism of NNIs in the livers of raccoons might be low. Our results contribute to a better understanding of the effects of NNIs on raccoons, leading to better conservation efforts for wild mammals. Environ Toxicol Chem 2022;41:1865–1874. © 2022 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.
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