Lead, inhalable particles

Radford, E. P., and E. A. Martell, Polonium-210 lead-210 ratios as an index of residence times of insoluble particles from cigarette smoke in bronchial epithelium, in Inhaled Particles IV, Part 2 (W. H. Walton, ed.) pp. 567-580, Pergamon Press, Oxford (1977). 

Inhalation. Ready absorption of lead-rich fumes, volatile organic lead compounds, or soluble lead-rich particles. 

Lead intake in mammals is caused by both food ingestion and inhaled air containing lead-bearing particles and aerosols. The latter pathway is a two-stage process the deposition of very small lead-bearing materials in the lungs and then the absorption of the metal which ultimately enters the bloodstream. 

The absorption of zinc oxide fumes lead to increased levels of zinc measured in the liver, kidney, and pancreas of cats exposed to zinc oxide fumes for durations ranging from 15 minutes to 3.25 hours (Drinker and Drinker 1928). The usefulness of the study is limited because reporting was inadequate and particle size of the zinc oxide aerosol was not determined. Some inhaled particles of zinc oxide are subject to ciliary clearance and swallowing. Thus, a portion of the inhaled zinc may ultimately be absorbed from the gastrointestinal tract. 

Monchaux, G., M. Morin, J.P. Morlier, and M.F. Olivier. 1997. Long-term effects of combined exposure to fission neutrons and inhaled lead oxide particles in rats. Arm. Occup. Hyg. 41(suppl. l) 630-635. 

Lead concentrations of 3-4 pg/m have been reported for residential areas (Las Lomas) and up to 14.5 pg/m for highly industrialized zones such as Xalostoc (see Fig. 4) (Bravo 1987). Besides, in one study, more than 30% of the lead was found in inhalable particles smaller than 1.1 pm in diameter (Espinoza 1985 cited by Cortinas 1988). These results agree with those from Grana-Garcia shown in Table 7 and indicate a potentially severe public health problem in the... 

Inhaled particles that are deposited on alveolar surfaces reduce their effective area, could cause significant damages to the surrounding tissues, and may even lead to cancer and serious heart problems. In this section, the process of particulate pollutant deposition in alveolar cavities is reviewed. Particular attention is given to computational modeling approach. 

Lead inhalation can occur when particle sizes are below 10 pm (micrometers) in diameter, as is the case with fiunes and line dust (World Health Organization 2010). Lead-polluted air results from lead smelter emissions and car emissions in countries that still use leaded gasoUne. Lead fiunes are also produced when heat guns are used to remove lead-based paint. 

Environment Canada has collected inhalable partides (<10 pm in diameter) in 15 Canadian cities since May 1984. Restdts for the period from May 1984 to December 1987 show that average inhalable particulate levels ranged fi om 17 pg/m in St. John s to 49 pg/m at a site in Montreal. Analysis has shown that the finest of the inhalable particles— those with a diameter less than about 2.5 pm— are different in origin and composition from the coarser particles in the 2.5- to 10-pm-diameter range. The coarse particles are mostly of natural origin (minerals from Earth s crust, sea salt, and plant material), whereas the fine particles consist of lead, sulfates, nitrates, carbon, and a variety of organic compoimds, mainly resulting from man-made pollution. At eastern Canadian sites, fine particulate matter accounted for more than 60 percent of the inhalable particles at sites in the Prairie provinces, the fine fraction was usually less than 40 percent of the inhalable particles. 

The interaction of inhaled particles, including CAPs, with macrophages leads to the production of ROS. ROS may further trigger the release of proin-flammatory cytokines and araehidonic acid metabolites (47). These inflammatory mediators, inflammatory cytokines, and especially ROS may be responsible for adverse effects of CAPs, such as pulmonary inflammation, airway narrowing, and increased morbidity and mortality. 

The greater bronchoconstrictive changes histologically and in measured pulmonary function in the chronic bronchitic animals combined with the more severe pulmonary inflammation solidified the hypothesized effect of inhaled particles. Extrapolating from these data, it is possible that the pulmonary inflammation causes changes in pulmonary function and the subsequent release of cytokines and other inflammatory mediators, which leads to cardiac alterations. 

It is also evident that inhaled particles and irritants, such as ozone and SO2, can cause perturbations in both the lungs and the cardiovascular system that can potentially contribute to the increased morbidity and mortality observed with increasing levels of these pollutants. There is httle doubt that these neural responses to inhaled irritants and antigen are increased in persons with hypersensitive airways, pulmonary congestion, and heart disease. Clearly, the roles of these irritants and allergens on these vital pulmonary and cardiovascular functions as well as the mechanisms whereby they defend the body or compromise its function need further delineation. This will help provide the needed mechanistic links between inhaled irritants and increased morbidity and mortality. In addition, it will lead to the identification of target sites for prophylactic and therapeutic intervention. 

Thus, several lines of evidence suggest that persons in the population at risk Irom inhaled particles are those with severe heart and lung diseases. The newer findings mirror the historical record from times of much higher exposures. In the London fog of 1952, the proportion of deaths attributed to heart and lung diseases increased during the dates of the fog (21). Additionally, because heart disease is the leading cause of death in the United States, any effect of particulate air pollution on total mortality would be expected to reflect at least an adverse effect on persons with heart disease. 

Inhaled tetraethyl and tetramethyl lead vapors behave as gases in the respiratory tract and, as a result, their pattern and extent of deposition and absorption differ from that of inhaled inorganic lead particles (EPA 1994a Overton et al. 1987 Overton and Miller 1988). These differences result in a higher fractional absorption of inhaled tetraethyl and tetramethyl lead (Heard et al. 1979). 

People living near hazardous waste sites may be exposed to lead via ingestion of contaminated water or soils or by inhalation of lead particles in the air. For people not living in the vicinity of hazardous waste sites, the major route of exposure to lead is ingestion, particularly of lead-contaminated water, food, soil, lead-based paint chips, or dusts (the latter two are particularly relevant to children in lower-income urbanized populations). For occupationally exposed individuals, the predominant route of exposure is the inhalation of lead particles with oral ingestion also important in many cases. 

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