1.Occupational Exposure to Metals in Shooting Ranges: A Biomonitoring Study
Eline VANDEBROEK ; Vincent HAUFROID ; Erik SMOLDERS ; Luc HONS ; Benoit NEMERY
Safety and Health at Work 2019;10(1):87-94
BACKGROUND: Lead (Pb) exposure in shooting ranges has been reduced by various measures such as jacketed ammunition and lead-free primers. Nevertheless, this may lead to exposure to other metals, potentially resulting in adverse health effects. METHODS: In a cross-sectional study, 35 subjects from seven different shooting ranges were studied: four shooting instructors, 10 police officers, 15 Special Forces, and six maintenance staff members. Metals and metalloids were determined in blood and urine by inductively coupled plasma–mass spectrometry. RESULTS: The concentrations of most elements did not differ significantly between groups or compared to reference values, except for Sb and Pt in urine and Pb in blood. Mean values for Sb were considerably higher in urine from the Special Forces (0.34 μg/L), the maintenance staff (0.13 μg/L), and shooting instructors (0.32 μg/L) compared to the police officers before shooting (0.06 μg/L) and a Belgian reference value (0.04 μg/L). For Pt, the Special Forces showed higher mean urinary concentrations (0.078 μg/L) compared to a Belgian reference value (<0.061 μg/L). Mean values for blood lead were markedly higher in the Special Forces (3.9 μg/dL), maintenance staff (5.7 μg/dL), and instructors (11.7 μg/dL) compared to police officers (1.4 μg/dL). One instructor exceeded the biological exposure index for blood Pb (38.8 μg/dL). CONCLUSION: Since both Pb and Sb were found to be higher in shooting range employees, especially among frequent shooters, it is advisable to provide appropriate protective equipment, education, and medical follow-up for shooting range personnel in addition to careful choice of ammunition.
Cross-Sectional Studies
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Education
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Environmental Monitoring
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Follow-Up Studies
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Humans
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Metalloids
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Metals
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Occupational Exposure
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Occupational Health
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Police
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Reference Values
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Spectrum Analysis
2.Skin Exposure Contributes to Chemical-Induced Asthma: What is the Evidence? A Systematic Review of Animal Models
Hung-Chang TSUI ; Steven RONSMANS ; Laurens J De SADELEER ; Peter H. M. HOET ; Benoit NEMERY ; Jeroen A. J. VANOIRBEEK
Allergy, Asthma & Immunology Research 2020;12(4):579-598
It is generally assumed that allergic asthma originates primarily through sensitization via the respiratory mucosa, but emerging clinical observations and experimental studies indicate that skin exposure to low molecular weight (LMW) agents, i.e. “chemicals,” may lead to systemic sensitization and subsequently develop asthma when the chemical is inhaled. This review aims to evaluate the accumulating experimental evidence that adverse respiratory responses can be elicited upon inhalation of an LMW chemical sensitizer after previous sensitization by dermal exposure. We systematically searched the PubMed and Embase databases up to April 15, 2017, and conducted forward and backward reference tracking. Animal studies involving both skin and airway exposure to LMW agents were included. We extracted 6 indicators of “selective airway hyper-responsiveness” (SAHR)—i.e. respiratory responses that only occurred in previously sensitized animals—and synthesized the evidence level for each indicator into strong, moderate or limited strength. The summarized evidence weight for each chemical agent was graded into high, middle, low or “not possible to assess.” We identified 144 relevant animal studies. These studies involved 29 LMW agents, with 107 (74%) studies investigating the occurrence of SAHR. Indicators of SAHR included physiological, cytological/histological and immunological responses in bronchoalveolar lavage, lung tissue and airway-draining lymph nodes. Evidence for skin exposure-induced SAHR was present for 22 agents; for 7 agents the evidence for SAHR was inconclusive, but could not be excluded. The ability of a chemical to cause sensitization via skin exposure should be regarded as constituting a risk of adverse respiratory reactions.
3.Skin Exposure Contributes to Chemical-Induced Asthma: What is the Evidence? A Systematic Review of Animal Models
Hung-Chang TSUI ; Steven RONSMANS ; Laurens J De SADELEER ; Peter H. M. HOET ; Benoit NEMERY ; Jeroen A. J. VANOIRBEEK
Allergy, Asthma & Immunology Research 2020;12(4):579-598
It is generally assumed that allergic asthma originates primarily through sensitization via the respiratory mucosa, but emerging clinical observations and experimental studies indicate that skin exposure to low molecular weight (LMW) agents, i.e. “chemicals,” may lead to systemic sensitization and subsequently develop asthma when the chemical is inhaled. This review aims to evaluate the accumulating experimental evidence that adverse respiratory responses can be elicited upon inhalation of an LMW chemical sensitizer after previous sensitization by dermal exposure. We systematically searched the PubMed and Embase databases up to April 15, 2017, and conducted forward and backward reference tracking. Animal studies involving both skin and airway exposure to LMW agents were included. We extracted 6 indicators of “selective airway hyper-responsiveness” (SAHR)—i.e. respiratory responses that only occurred in previously sensitized animals—and synthesized the evidence level for each indicator into strong, moderate or limited strength. The summarized evidence weight for each chemical agent was graded into high, middle, low or “not possible to assess.” We identified 144 relevant animal studies. These studies involved 29 LMW agents, with 107 (74%) studies investigating the occurrence of SAHR. Indicators of SAHR included physiological, cytological/histological and immunological responses in bronchoalveolar lavage, lung tissue and airway-draining lymph nodes. Evidence for skin exposure-induced SAHR was present for 22 agents; for 7 agents the evidence for SAHR was inconclusive, but could not be excluded. The ability of a chemical to cause sensitization via skin exposure should be regarded as constituting a risk of adverse respiratory reactions.