Respiratory effect

A distinct relation between parental occupational exposure and childhood cancer was shown for solvents and paints. High parental exposure resulted in higher incidences of childhood cancers. In the same study, however, generally more cancers were found as a result of parental use of alcohol and tobacco smoke. Childhood leukemia and nervous system cancers, in particular, are the types suspected to be caused by parental exposure to paints and solvents. Kishi et al. described an elevated risk for acute lymphatic leukemia in children of mothers with prenatal exposures to benzene and to paints. In former studies with small numbers of children these tendencies could also be shown, mainly in male painters whose children showed a higher incidence of childhood leukemia and brain tumors. 18.3.4.2.4 Respiratory effects 

Irritations of the air passages were described in people exposed to fumes in paint fac- 

VOCs in paints can provoke respiratory symptoms (wheezing, breathlessness) in asthmatics. Conventional water-based paints with only small amounts of VOCs have also been shown to cause such symptoms, but there were no effects using VOC-free paints. No differences were found in the same study looking at lung function and airway responsiveness. Toxic pyrolysis products in paints and polymer films probably evoke asthma-like symptoms similar to PVC pyrolysis.  

A decrease in forced vital capacity, expiratory volume in one second and of peak exspiratory flow was observed after exposure to water-based paints. Bronchial obstruction in painters was confirmed by White and Baker, but other studies could not detect changes in lung function parameters in house painters who were exposed to solvent-based and water-based paints. Beving et al. did not find obstmctive effects in car painters. An increase 

Histological changes in the nasal mucosa of spray painters were also noted in a study of Hellquist et al.  

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Some nonmalignant respiratory effects have been observed in experimental animals during acute or subchronic exposures. Soluble and moderately soluble compounds were more toxic than were insoluble compounds and produced different effects. Sulfate and subsulftde produced fibrosis whereas nickel oxide did not. 

It is good practice to keep concentrations of airborne nickel in any chemical form as low as possible and certainly below the relevant standard. Local exhaust ventilation is the preferred method, particularly for powders, but personal respirator protection may be employed where necessary. In the United States, the Occupational Safety and Health Administration (OSHA) personal exposure limit (PEL) for all forms of nickel except nickel carbonyl is 1 mg/m. The ACGIH TLVs are respectively 1 mg/m for Ni metal, insoluble compounds, and fume and dust from nickel sulfide roasting, and 0.1 mg/m for soluble nickel compounds. The ACGIH is considering whether to lower the TLVs for all forms of nickel to 0.05 mg/m, based on nonmalignant respiratory effects in experimental animals. 

Desflurane is less potent than the other fluorinated anesthetics having MAC values of 5.7 to 8.9% in animals (76,85), and 6% to 7.25% in surgical patients. The respiratory effects are similar to isoflurane. Heart rate is somewhat increased and blood pressure decreased with increasing concentrations. Cardiac output remains fairly stable. Desflurane does not sensitize the myocardium to epinephrine relative to isoflurane (86). EEG effects are similar to isoflurane and muscle relaxation is satisfactory (87). Desflurane is not metabolized to any significant extent (88,89) as levels of fluoride ion in the semm and urine are not increased even after prolonged exposure. Desflurane appears to offer advantages over sevoflurane and other inhaled anesthetics because of its limited solubiHty in blood and other tissues. It is the least metabolized of current agents. 

Respiratory effect. The minimal, effective, depressant dose as measured by Wright and Barbour s method. ... 

Consideration of hygiene (toxicological, dermatological and respiratory effects) ... 

Common adverse effects include headache, nausea, diarrhea, anorexia, rhinitis, and flu-like symptoms. The most serious adverse reactions are related to respiratory effects and include severe bronchospasm that may lead to death. 

Respiratory Effects. Pulmonary edema was reported in humans dying from acute methyl parathion (Wofatox) intoxication (Fazekas 1971). Edema was found in a man who died 2 hours after intoxication, and, in other cases, edema was found in others who died as long as 9 days after exposure. Broncho-constriction and hypersecretion of bronchial glands (bronchorrhea) are primary muscarinic effects of methyl parathion. The broncoconstriction, bronchorrhea, and bradycardia caused by methyl parathion are strongly conducive to pulmonary edema. 

Routine gross and histopathological examinations revealed no treatment-related effects on the respiratory system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 1981). Chronic dietary exposure to methyl parathion did not induce respiratory effects in mice fed 16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

LOAEL A Lowest-Observed-Adverse-Effeet Level (LOAEL) is the lowest dose used in the study that caused a harmful health effect. LOAELs have been classified into "Less Serious" and "Serious" effects. These distinctions help readers identify the levels of exposure at which adverse health effects first appear and the gradation of effects with increasing dose. A brief description of the specific end point used to quantify the adverse effect accompanies the LOAEL. The respiratory effect reported in key number 18 (h q)erplasia) is a Less serious LOAEL of 10 ppm. MRLs are not derived from Serious LOAELs. 

Respiratory Effects. No studies were located regarding respiratory effects in humans after inhalation exposure to endosulfan. 

Respiratory Effects. Increased occurrence of dyspnea and increased respiratory rate were noted in 18 agricultural workers in India who applied endosulfan without protective equipment (both dermal and inhalation exposures probably occurred) (Chugh et al. 1998). 

Respiratory Effects. No reports were located indicating that endosulfan is a significant respiratory irritant. However, respiratory effects (e.g., hypoxia, dyspnea, and cyanosis) have been observed in... 

Respiratory Effects. A worker developed labored breathing and respiratory edema after welding stainless steel that had been washed in trichloroethylene (Sjogren et al. 1991). The effects were attributed to inhalation of the trichloroethylene decomposition products phosgene and diehloroacetyl chloride, although a history of cigarette smoking may have predisposed the subjeet to these respiratory effects. 

Respiratory Effects. One study suggested increased respiratory disorders (asthma, bronchitis, pneumonia) in children with chronic exposure to a solvent-contaminated water supply (Byers et al. 1988). Two municipal wells in eastern Woburn, Massachusetts, were found to contain several solvents including trichloroethylene (267 ppb) and tetrachloroethylene (21 ppb). The increased susceptibility to infection may be secondary to effects on the immune system. Accurate chemical-specific exposure levels for individuals could not be determined because the water distribution system was designed to use water from different wells at different rates and times. Other limitations of this study are described in Section 2.2.2.8. 

Rales and dyspnea were observed in pregnant rats treated by gavage with 1,500 mg/kg/day trichloroethylene in com oil on gestation days 6-19 (Narotsky and Kavlock 1995). Respiratory effects were not observed at 1,125 mg/kg/day. Pulmonary vasculitis was observed in 6 of 10 female rats treated with 1,000 mg/kg/day (by gavage) and 6 of 10 male rats treated with 2,000 mg/kg/day (in com oil) for 13 weeks (NTP 1990). This effect was also observed in 1 of 10 male and 1 of 10 female control rats. Histopathological examinations were not completed at the other doses in this study. Therefore, it is not possible to determine if this is a dose-related effect. 

Additional studies of the Woburn population have been completed (MDPH 1994). The final report indicated that there was an increased prevalence in choanal atresia, a rare respiratory effect, and hypospadias/congenital chordee. A small increase in eye defects was observed, but there was no association between TCE exposure and heart defects. There was no statistically significant associations between exposure concentrations and birth defects, although analyses was limited by the small number of cases observed. Based on four cases in the Woburn population, a rate of 0.88 was observed in the exposed population, compared to rates of 0.11 and 0.13 in the Atlanta and California comparison populations, respectively. In a prospective study completed after well closure, the rate of choanal atresia was 0.88 (based on 1 case) in Woburn, 0.11 in the surrounding communities, and 0.2 and 0.13 in Atlanta and California, respectively. The study authors cautioned that their study did not rule out moderate increases in rates of the less common adverse reproductive outcomes. For these outcomes only large increases would have been detected. 

Some members of a community that were exposed to trichloroethylene along with a variety of other solvents in their drinking water complained of respiratory disorders, but the complaints could not be attributed specifically to trichloroethylene (Byers et al. 1988). This effect may have been due to immune system impairment resulting in increased susceptibility to infection. A study in mice in which inhalation exposure to trichloroethylene increased the susceptibility to pulmonary infection with Streptococcus zooepidemicus (Aranyi et al. 1986) provides evidence that trichloroethylene may result in adverse respiratory effects through effects on the immune system. 

The large numbers of opioid receptors in areas of the brainstem such as the solitary tract and adjacent areas are probably related to respiratory effects of opiates, cough suppression and nausea and vomiting. Opiates acting in the brainstem reduce the sensitivity of the respiratory centres to pC02 and this is the most common cause of death from overdose with street use of opiates. 

Respiratory Effects. Inhalation exposure of dogs to 241 Am resulted in respiratory insufficiency and pneumonia as well as histopathologic changes in the lungs. Inhalation exposure of rats resulted in radiation pneumonitis. 

No data were located regarding respiratory effects, cardiovascular effects, gastrointestinal effects, hepatic effects, renal effects, endocrine effects, dermal effects, ocular effects, body weight effects, or metabolic effects in humans or animals following acute-, intermediate-, or chronic-duration dermal exposure to americium ... 

The respiratory system does not appear to be a target of diisopropyl methylphosphonate. Exposure has only occasionally resulted in respiratory effects, and the effects did not appear to be dose or treatment related. Necropsy of both male and female rats that died as the result of a single dose (928, 1,362, or... 

In a study of calves dosed with diisopropyl methylphosphonate at 62.5, 125, 250, 500, or 1,000 mg/kg via gelatin capsules placed with a balling gun, calves at the highest dose level displayed pulmonary emphysema upon autopsy (Palmer et al. 1979). No respiratory effects were observed at sublethal dose levels. 

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