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PubMed1995

Aerosol deposition as a function of airway disease: cystic fibrosis.

A mathematical model of aerosol deposition has been developed for drug delivery protocols and used successfully to simulate inhalation exposure tests with human subjects. Therefore, we have used the validated model to address the delivery of inhaled pharmaceuticals as a function of disease-induced changes in airway structure. Clinical data from the literature had suggested that progressive lung disease associated with cystic fibrosis (CF) could compromise the successful administration of pharmacologic drugs used in its treatment, hence it was studied. We described the lungs of patients inflicted with CF by different morphologies (representing the processes of airway obstruction, infection and inflammation) than healthy (control) subjects. Affected ventilatory parameters were also examined to demonstrate their effects upon drug disposition. Particle distributions were computed on a generation-by-generation basis. Deposition patterns were dramatically affected by CF-produced alterations in dimensions. The reduced airway caliber in CF enhanced the total dose delivered to the tracheobronchial compartment by 200-300% relative to controls. The spatial distributions of aerosols were completely different in CF patients, being selectively deposited within congested airways. In medical practice the model can be tailored to any specific airway disease. Regarding targeted delivery, the results have relevance to (1) site-specific acting pharmaceuticals in tracheobronchial airways and (2) drugs designed for systemic delivery via deposition in alveolated airways.

Administration, Inhalation↗
PubMed2006

Review of the evidence regarding the carcinogenicity of hexavalent chromium in drinking water.

Recent analyses have revealed that 38% of municipal sources of drinking water in California have detectable levels of hexavalent chromium. This observation provided new impetus to characterize the carcinogenic risk associated with oral exposure to hexavalent chromium in drinking water. Notwithstanding the well-characterized increases in cancer associated with inhalation exposure to this chemical, the marked reduction of hexavalent chromium to trivalent chromium in the stomach suggests that exposure to hexavalent chromium in drinking water may not pose a carcinogenic risk. A reevaluation of studies that investigated the toxicokinetics, the genotoxicity, and the mechanism of carcinogenicity of hexavalent chromium, as well as the available human and animal cancer studies, was undertaken to determine if there is evidence that exposure to this chemical in drinking water may pose a carcinogenic risk. Mechanistic studies suggest the potential for a carcinogenic response if hexavalent chromium enters cells. Both toxicokinetic and genotoxicity studies indicate that a portion of an orally administered dose of hexavalent chromium is absorbed and gets into cells of several tissues, causing DNA damage. The only lifetime oral study of hexavalent chromium in animals conducted thus far yielded a statistically significant increase in stomach tumors compared to controls. Also, in a limited-term cancer study, co-exposure to hexavalent chromium in drinking water and ultraviolet light produced skin tumors in mice. The only available cancer study of humans exposed to hexavalent chromium in drinking water revealed a statistically significant increase in stomach tumors. Moreover, a meta-analysis of occupational studies also revealed a statistically significant increase in stomach cancers. The increases in stomach tumors in both human and animal studies, along with the toxicokinetic, genotoxic, and mechanistic data, suggest that oral exposure to this agent appears to pose a carcinogenic risk.

Animals↗
PubMed1997

Aluminum exposure and metabolism.

Aluminum (Al) is a nonessential, toxic metal to which humans are frequently exposed. Oral exposure to aluminum occurs through ingestion of aluminum-containing pharmaceuticals and to a lesser extent foods and water. Parenteral exposure to aluminum can occur via contaminated total parenteral nutrition (TPN), intravenous (i.v.) solutions, or contaminated dialysates. Inhalation exposure may be important in some occupational settings. The gut is the most effective organ in preventing tissue aluminum accumulation after oral exposure. Typically gastrointestinal absorption of aluminum from diets is < 1%. Although the mechanisms of aluminum absorption have not been elucidated, both passive and active transcellular processes and paracellular transport are believed to occur. Aluminum and calcium may share some absorptive pathways. Aluminum absorption is also affected by the speciation of aluminum and a variety of other substances, including citrate, in the gut milieu. Not all absorbed or parenterally delivered aluminum is excreted in urine. Low glomerular filtration of aluminum reflects that most aluminum in plasma is nonfiltrable because of complexation to proteins, predominantly transferrin. The importance of biliary secretion of aluminum is debatable and the mechanism(s) is poorly understood and appears to be saturable by fairly low oral doses of aluminum.

Absorption↗
PubMed1990

Treated vs reported toxic exposures: discrepancies between a poison control center and a member hospital.

Statistics accumulated by Poison Control Centers (PCC) are routinely used on the local, regional and national levels by governmental agencies to set policy and direct funding. Incomplete reporting by member hospitals is recognized by PCC as a factor contributing to discrepancies in epidemiological estimates; however little emphasis is classically placed by the PCC on expanding reporting from member hospitals. A 1y retrospective review of patients with toxic exposure presenting to an urban Emergency Medicine Department (EMD) was performed to quantify the lack of concordance between treated and reported toxic exposures. 470 toxic exposures presented over the study period, of which only 123 (26%) were relayed to the regional PCC. Inhalation exposures were least likely to be referred for PCC consultation (3%); whereas PCC consultation was obtained for 33% venomous snake bite cases, and 95% of the cyclic antidepressant ingestions. Clusters of similar exposures resulted in fewer PCC consultations. Understanding each hospital's "profile" for handling toxic exposures, and individualized advertisement by the PCC to their member hospital may increase their data reporting. The statistical significance of their epidemiological studies as well as their revenue may increase.

Environmental Exposure↗
PubMed1996

Effect of radon on the immune system: alterations in the cellularity and functions of T cells in lymphoid organs of mouse.

Exposure to radon and its progeny induces significant damage to the cells of the respiratory tract and causes lung cancer. Whether a similar exposure to radon would alter the functions of the immune system has not been previously investigated. In the current study, we investigated the effect of exposure of C57BL/6 mice to 1000 or 2500 working-level months (WLM) of radon and its progeny by inhalation, on the number and function of T lymphocytes in lymphoid organs. The control mice received uranium ore dust carrier aerosol by inhalation. Exposure to radon induced marked decrease in the total cellularity of most lymphoid organs such as thymus, peripheral lymph nodes (PLN), and lung-associated lymph nodes (LALN), when compared to the controls. The percentage of T cells increased, while that of non-T cells decreased, in all peripheral lymphoid organs at both the doses of radon. In the thymus, particularly at 2500 WLM of radon exposure, there was a marked decrease in CD4+CD8+ T cells and an increase in the immature CD4-CD8- T cells. Such alterations in both the numbers and percentages of lymphocytes and macrophages in radon-exposed mice may have resulted from the cell killing by the alpha particles as the immune cells were migrating through the lungs, or it may have been caused by altered migration of cells, inasmuch as expression of CD44, a molecule involved in migration and homing of immune cells, was significantly altered on cells found in different lymphoid organs. In the LALN, where one would predict the largest number of damaged cells to be present, there was a significant decrease in the T-cell responsiveness to mitogens while the B-cell response was not affected. Such alterations may have resulted from the direct effect of alpha-particle exposure on the migrating lymphocytes, altered percentage of lymphocytes as seen in secondary lymphoid organs, or altered expression of adhesion molecules involved in cell activation such as CD44 and CD3. Interestingly, radon exposure caused and increase in the T- and B-cell responsiveness to mitogens in the spleen and PLN. Since there is little evidence of direct radiation dose from radon in lymphoid organs, our studies demonstrating immunological alterations suggest an indirect effect of radon exposure that may have significant repercussions on the development of hypersensitivity and increased susceptibility to infections and cancer in the lung.

Administration, Inhalation↗
PubMed1996

Ingestion, inhalation, and dermal exposures to chloroform and trichloroethene from tap water.

Individuals are exposed to volatile compounds present in tap water by ingestion, inhalation, and dermal absorption. Traditional risk assessments for water often only consider ingestion exposure to toxic chemicals, even though showering has been shown to increase the body burden of certain chemicals due to inhalation exposure and dermal absorption. We collected and analyzed time-series samples of expired alveolar breath to evaluate changes in concentrations of volatile organic compounds being expired, which reflects the rate of change in the bloodstream due to expiration, metabolism, and absorption into tissues. Analysis of chloroform and trichloethene in expired breath, compounds regulated in water, was also used to determine uptake from tap water by each route (inhalation, ingestion, or absorption). Each route of exposure contributed to the total exposure of these compounds from daily water use. Further, the ingestion dose was completely metabolized before entering the bloodstream, whereas the dose from the other routes was dispersed throughout the body. Thus, differences in potential biologically effective doses depend on route, target organ, and whether the contaminant or metabolite is the biologically active agent.

Adult↗
PubMed1989

Pulmonary immune response of dogs after exposure to 239PuO2.

This study evaluated the cell-mediated (CMI) and humoral immune responses in four Beagle dogs five to six years after single inhalation exposures to different monodisperse 239PuO2 aerosols (0.72-1.4 microns activity median aerodynamic diameter). These exposures resulted in initial lung burdens ranging from 19 to 35 kBq. Four nonexposed dogs were used as age-matched controls. Anesthetized dogs were immunized by instillation of sheep red blood cells (SRBC) into selected lung lobes. Cells and fluids were obtained serially from blood samples and by bronchoalveolar lavage of the saline- and SRBC-treated lung lobes at 5-20 days after immunization. The CMI response evaluated by the leukocyte procoagulant activity test was similar in the saline- and SRBC-treated lobes of both groups of dogs. The humoral immune response was measured by the enzyme-linked immunosorbent assay. No differences were shown between the amount of antibody measured in the sera or lung lavages from control or Pu-exposed dogs. Histopathology of the tracheobronchial lymph nodes from the Pu-exposed dogs showed them to be fibrotic with no lymphoid cells, suggesting that these tissues could not respond to the antigen deposited in the lungs. However, both mediastinal and sternal lymph nodes did contain lymphoid tissue, and were likely to be the lymphoid tissues that produced the immunity to the antigen deposited in the lungs of the exposed dogs. Although both exposed and control dogs produced immune responses to the antigen instilled into their lungs, differences were observed in the number of neutrophils in lung lavages from the control and exposed animals. There was a dramatic influx of neutrophils into both the saline- and SRBC-treated lung lobes of the Pu-exposed dogs that was not seen in the age-matched controls. This suggests that the inhaled 239PuO2 produced chronically-active inflammation in the lung which may contribute to recruitment of lymphocytes to the lung following intrapulmonary deposition of antigen. In conclusion, the immune responses induced by lung immunization of dogs that had inhaled 239PuO2 were not suppressed by large doses of chronic alpha irradiation of the lungs and tracheobronchial lymph nodes, indicating that local pulmonary immune responses are preserved despite severe radiation-induced alteration of these tissues.

Administration, Inhalation↗
PubMed1985

Developmental effects associated with exposure to xylene: a review.

Data obtained from rodents indicates that maternal exposure to mixed xylenes or individual xylene isomers can have adverse effects on the conceptus. Fetotoxic effects were reported following maternal inhalation exposure to mixed xylenes; altered enzyme activities were also found in rat pups. Dermal application resulted in apparent changes in fetal enzyme activities, while oral treatment was followed by prenatal mortality, growth inhibition, and malformations, primarily cleft palate. Maternal inhalation of individual isomers was associated with all of the above mentioned effects, with the exception of cleft palate. The o- and p-isomers appeared more hazardous to offspring than did the m-isomer. Malformations (i.e., cleft palate) associated with mixed or individual isomers were primarily reported at maternally toxic doses. Thus, a clear case for a selective teratogenic effect due to exposure to xylene has yet to be presented.

Animals↗
PubMed2006

Enhancement of renal carcinogenicity by combined inhalation and oral exposures to chloroform in male rats.

Chloroform, ubiquitously present in indoor and outdoor air, drinking water, and some foodstuffs, enters the human body by inhalation, oral and dermal routes of exposure. In order to provide bioassay data for risk assessment of humans exposed to chloroform by multiple routes, effects of combined inhalation and oral exposures to chloroform on carcinogenicity and chronic toxicity in male F344 rats were examined. A group of 50 male rats was exposed by inhalation to 0 (clean air), 25, 50, or 100 ppm (v/v) of chloroform vapor-containing air for 6 h/d and 5 d/wk during a 104 w period, and each inhalation group was given chloroform-formulated drinking water (1000 ppm w/w) or vehicle water for 104 wk, ad libitum. Renal-cell adenomas and carcinomas and atypical renal-tubule hyperplasias were increased in the combined inhalation and oral exposure groups, but not in the oral- or inhalation-alone groups. Incidences of cytoplasmic basophilia and dilated tubular lumens in the kidney, as well as incidence of positive urinary glucose, were markedly increased by the combined exposures, compared with those after single-route exposures. It was concluded that combined inhalation and oral exposures markedly enhanced carcinogenicity and chronic toxicity in the proximal tubule of male rat kidneys, suggesting that carcinogenic and toxic effects of the combined exposures on the kidneys were greater than the ones that would be expected under an assumption that the two effects of single route exposures through inhalation and drinking were additive.

Administration, Oral↗
PubMed2001

Respiratory tract toxicity in rats exposed to Mexico City air.

The rat has been used extensively as a health sentinel, indicator, or monitor of environmental health hazards, but this model has not been directly validated against human exposures. Humans in Mexico City show upper respiratory tract lesions and evidence of pulmonary damage related to their environmental inhalation exposure. In this study, male and female F344 rats were exposed (23 hr/day) in Mexico City to local Mexico City air (MCA)* for up to seven weeks. Controls were maintained at the same location under filtered air. Prior to these exposures, several steps were taken. First, the nasal passages of normal male rats shipped from the United States and housed in Mexico City were examined for mycoplasma infection; no evidence of infection was found. In addition, a mobile exposure and monitoring system was assembled and, with an ozone (O3) exposure atmosphere, was tested along with supporting histopathology techniques and analysis of rat nasal and lung tissues. Last, the entire exposure model (equipment and animals) was transported to Mexico City and validated for a three-week period. During the seven-week study there were 18 one-hour intervals during which the average O3 concentration of MCA in the exposure chamber exceeded the US National Ambient Air Quality Standard (NAAQS) of 0.120 ppm 03 (hourly average, not to be exceeded more than once per year). This prolonged exposure of healthy F344 rats to MCA containing episodically low to moderate concentrations of 03 (as well as other urban air pollutants) did not induce inflammatory or epithelial lesions in the nasal airways or lung as measured by qualitative histologic techniques or quantitative morphometric techniques. These findings agree with those of previous controlled O3 inhalation studies, but they are in contrast to reports indicating that O3-polluted MCA causes significant nasal mucosal injury in adults and children living in southwestern Mexico City. Taken together, these findings may suggest that human airways are markedly more susceptible to the toxic effects of MCA than are the airways of the F344 rat.

Air Pollutants↗
PubMed2001

A chronic inhalation toxicity/oncogenicity study of methylethylketoxime in rats and mice.

To evaluate the oncogenic potential of methylethylketoxime (MEKO), CD-1 mice (50/sex/group) and F-344 rats (50/sex/group) were coexposed 6 h/day, 5 days/wk for 18 mo (mice) or 26 mo (rats) via whole-body inhalation exposures to target vapor concentrations of 0, 15, 75, and 375 ppm (actual concentrations of 0, 15 +/- 1, 75 +/- 2, or 374 +/- 10 ppm). Satellite groups of rats and mice (10/sex/group/interval) were exposed for 12 mo (mice) and 3, 12, or 18 mo (rats) to evaluate chronic toxicity. Methyl ethyl ketone (MEK), a possible hydrolysis product of MEKO, was present at less than 1%. Treatment-related effects included increased body weight (male rats only), methemoglobin formation, hematology and clinical chemistry changes, increased liver weight, and increased spleen and testes weights (rats only). A high incidence of cataracts and corneal dystrophy occurred in both control and MEKO-exposed rats, with an earlier appearance and slightly higher incidence for these ocular lesions in MEKO-exposed animals compared to controls. Degenerative and reparative changes of the olfactory epithelium in the nasal turbinates, primarily limited to the dorsal meatus, occurred in both rats (75 and 374 ppm) and mice (15, 75, and 374 ppm). In addition, in the mice, liver changes included increased incidences of pigment in reticuloendothelial cells, centilobular hypertrophy, granulomatous inflammation, and a slightly increased incidence of necrosis (75 and 374 ppm). An increase in hepatocellular carcinomas occurred in male mice at 374 ppm. Additional MEKO-related findings in the rat included congestion of the spleen with pigment in reticuloendothelial cells and extramedullary hematopoiesis and a decreased incidence of lymphoreticular mononuclear cell leukemia. Effects observed in the liver of the rats included decreases in the incidence of both peribiliary fibrosis and hyperplasia/proliferation of the biliary duct, an increase of spongiosis hepatis in males, and an increase in the incidence of intracytoplasmic vacuoles and hepatocellular basophilic foci. The effects on the liver were generally most profound in the high-exposure groups and, with the exception of the spongiosis hepatis, occurred in both sexes. An increase in hepatocellular adenomas occurred in the male rats at 75 and 374 ppm, and hepatocellular carcinomas in the male rats at 374 ppm. In both species, the liver tumors appeared relatively late in the life of the animals, with no significant increase in tumors at 12 mo of exposure in mice and at 18 mo of exposure in rats. Lifespan shortening was not observed, as MEKO-exposed animals survived generally as well as, or slightly better than, the controls.

Administration, Inhalation↗
PubMed1985

Depletion of nasal mucosal glutathione by acrolein and enhancement of formaldehyde-induced DNA-protein cross-linking by simultaneous exposure to acrolein.

Incubation of homogenates of rat nasal mucosa with acrolein resulted in the apparent formation of DNA-protein cross-links. However, inhalation exposure of male Fischer-344 rats to acrolein (2.0 ppm, 6 h) did not cause detectable DNA-protein cross-linking in the nasal respiratory mucosa. Simultaneous exposure of rats to both acrolein (2.0 ppm) and formaldehyde (6.0 ppm) for 6 h resulted in a significantly higher yield of DNA-protein cross-links than was obtained following exposure to formaldehyde (6.0 ppm) alone. Acrolein exposure at concentrations of 0.1, 0.5, 1.0, or 2.5 ppm resulted in a concentration-dependent depletion of nonprotein sulfhydryl groups in the nasal respiratory mucosa. A plausible explanation for the enhancement of DNA-protein cross-links by simultaneous exposure to formaldehyde and acrolein may be that depletion of glutathione by acrolein inhibited the oxidative metabolism of formaldehyde, leading to an increase of formaldehyde-induced DNA-protein cross-links.

Acrolein↗
PubMed1986

[Cancerogenic effect of long-term benzene exposure. Occurrence at the same work place of a plasmacytoma and two solid carcinomas ].

A report is given on three different malignomas appearing after high inhalative exposure to benzene for many years at the same working place in a cable plant. The exposure to benzene amounted to 22 years in a 50 year old man with oesophagus carcinoma, 17 years in a 61 year old man with plasmocytoma and 10 years in a 45 year old man with embryonal carcinoma of the testicles. The malignomas appeared 5-7 years after the end of the exposure. The carcinogenity of benzene is discussed on the basis of a survey of medical literature on epidemiological studies, casuistic contributions and experimental investigations in animals. A direct and indirect mechanism of benzene inducing carcinogenity is discussed: Activation of normal cellular oncogenes in DNA molecules by changes directly caused by benzene and; Damage of the lymphatic cell particularly susceptible to benzene followed by a disturbance of immunological monitoring and defence reactions against tumour cells.

Air Pollutants, Occupational↗
PubMed1993

Inhalation toxicity of 1,6-hexanediamine dihydrochloride in F344/N rats and B6C3F1 mice.

1,6-Hexanediamine (HDA) is a high production volume chemical which is used as an intermediate in the synthesis of paints, resins, inks, and textiles and as a corrosion inhibitor in lubricants. Two- and 13-week studies of the toxicity of the dihydrochloride salt of HDA (HDDC) were conducted in male and female Fischer 344/N rats and B6C3F1 mice using whole-body inhalation exposure. Both species were evaluated for histopathologic and reproductive effects, and rats were examined for clinical chemistry and hematologic changes. In the 2-week inhalation studies, animals were exposed to 10-800 mg HDDC/m3, 6 hr per day. All rats, all female mice, and two of five male mice in the high-exposure group died before the end of the study. Surviving mice in this group had a dose-dependent depression in body weight gain. Clinical signs were primarily related to upper respiratory tract irritation and included dyspnea and nasal discharge in both species. Treatment-related histopathologic lesions included inflammation and necrosis of the laryngeal epithelium of both species and the tracheal epithelium of mice, as well as focal inflammation and ulceration of the respiratory and olfactory nasal mucosa. In the 13-week inhalation studies, animals were exposed to HDDC at concentrations of 1.6-160 mg/m3 for 6 hr per day, 5 days per week. In addition to the base study groups, a supplemental group of rats at each exposure level was included to assess the effect of HDDC on reproduction. No treatment-related changes in organ weights or organ-to-body-weight ratios occurred in rats, and no treatment-related clinical signs or gross lesions were seen in either species. Chemical-related microscopic lesions were limited to the upper respiratory tract (larynx and nasal passages) in the two highest exposure groups and were similar in both species. These lesions included minimal to mild focal erosion, ulceration, inflammation, and hyperplasia of the laryngeal epithelium, in addition to degeneration of the olfactory and respiratory nasal epithelium. HDDC caused no significant changes in sperm morphology or vaginal cytology and no significant adverse effects on reproduction in rats or mice. Hematologic and clinical chemistry changes in rats were minor and sporadic and were not accompanied by related histologic findings. HDDC did not increase the frequency of micronucleated erythrocytes in mice.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗
PubMed1990

Quantitative estimation of the genetic risk associated with the induction of heritable translocations at low-dose exposure: ethylene oxide as an example.

This paper explores how quantitative risk assessment methods might be extended to analysis of risks to the human germ line. High inhalation exposures to ethylene oxide are reported to cause heritable translocations in male mice with a steep and nonlinear dose-response-curve. We explore quantitative estimation of risk to humans from low exposures based on these animal data, addressing questions of tissue dosimetry for this alkylating agent, expected equivalency of doses across species, germ-cell sensitivity, and extrapolation of dose-response relationship to low exposure levels. Various dose-response models are discussed in terms of their applicability to genetic end points and their ability to reflect the underlying basis of induced heritable translocations.

Administration, Inhalation↗
PubMed1989

The effect of titanium dioxide inhalation on the pulmonary clearance of Pasteurella haemolytica in the mouse.

Four inhalation exposure chambers were designed and built in which up to 80 mice per chamber could be accommodated. Exposure for several weeks to an inert inorganic particulate aerosol of titanium dioxide at a respirable aerosol concentration of 20 mg m-3 impaired the clearance of Pasteurella haemolytica in proportion to the duration of exposure. Other groups exposed to a lower respirable concentration of 2 mg m-3 exhibited similar clearance rates relative to mice maintained in clean air. A recovery experiment showed that inhalation of TiO2 at 20 mg m-3 for 10 days impaired bacterial clearance at least 10 days after cessation of exposure to TiO2.

Administration, Inhalation↗
PubMed1980

The combined toxicity of technical grade xylene and ethanol in the rat.

1. Inhalation exposure to xylene of technical grade (300 p.p.m. in air, 6 h a day, 5 days a week, up to 18 weeks) enhanced the overall mono-oxygenation reactions (7-ethoxycoumarin O-deethylase and 2,5-diphenyloxazole hydroxylase( as well as the UDP-glucuronyltransferase activity in rat liver microsomes. 2. The simultaneous ingestion of aqueous 15-20% ethanol as drinking fluid increased the cytochrome P-450 concn. and the mono-oxygenation activity even more than the xylene exposure alone. 3. Xylene-ethanol treatment resulted in additive or less than additive effects on the measured hepatic enzyme activities. 4. Renal ethoxycoumarin deethylase activity was enhanced both by ethanol ingestion and by xylene inhalation, and the response was additive after the combined exposure. 5. Liver histology revealed that even though the xylene exposure alone did not produce detectable liver damage, the xylene-ethanol treatment produced more severe liver damage than did ethanol ingestion alone.

Animals↗
PubMed2003

Adverse human health effects associated with molds in the indoor environment.

Molds are common and important allergens. About 5% of individuals are predicted to have some allergic airway symptoms from molds over their lifetime. However, it should be remembered that molds are not dominant allergens and that the outdoor molds, rather than indoor ones, are the most important. For almost all allergic individuals, the reactions will be limited to rhinitis or asthma; sinusitis may occur secondarily due to obstruction. Rarely do sensitized individuals develop uncommon conditions such as ABPA or AFS. To reduce the risk of developing or exacerbating allergies, mold should not be allowed to grow unchecked indoors. When mold colonization is discovered in the home, school, or office, it should be remediated after the source of the moisture that supports its growth is identified and eliminated. Authoritative guidelines for mold remediation are available. Fungi are rarely significant pathogens for humans. Superficial fungal infections of the skin and nails are relatively common in normal individuals, but those infections are readily treated and generally resolve without complication. Fungal infections of deeper tissues are rare and in general are limited to persons with severely impaired immune systems. The leading pathogenic fungi for persons with nonimpaired immune function, Blastomyces, Coccidioides, Cryptococcus, and Histoplasma, may find their way indoors with outdoor air but normally do not grow or propagate indoors. Due to the ubiquity of fungi in the environment, it is not possible to prevent immunecompromised individuals from being exposed to molds and fungi outside the confines of hospital isolation units. Some molds that propagate indoors may under some conditions produce mycotoxins that can adversely affect living cells and organisms by a variety of mechanisms. Adverse effects of molds and mycotoxins have been recognized for centuries following ingestion of contaminated foods. Occupational diseases are also recognized in association with inhalation exposure to fungi, bacteria, and other organic matter, usually in industrial or agricultural settings. Molds growing indoors are believed by some to cause building-related symptoms. Despite a voluminous literature on the subject, the causal association remains weak and unproven, particularly with respect to causation by mycotoxins. One mold in particular, Stachybotrys chartarum, is blamed for a diverse array of maladies when it is found indoors. Despite its well-known ability to produce mycotoxins under appropriate growth conditions, years of intensive study have failed to establish exposure to S. chartarum in home, school, or office environments as a cause of adverse human health effects. Levels of exposure in the indoor environment, dose-response data in animals, and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations. Mold spores are present in all indoor environments and cannot be eliminated from them. Normal building materials and furnishings provide ample nutrition for many species of molds, but they can grow and amplify indoors only when there is an adequate supply of moisture. Where mold grows indoors there is an inappropriate source of water that must be corrected before remediation of the mold colonization can succeed. Mold growth in the home, school, or office environment should not be tolerated because mold physically destroys the building materials on which it grows, mold growth is unsightly and may produce offensive odors, and mold is likely to sensitize and produce allergic responses in allergic individuals. Except for persons with severely impaired immune systems, indoor mold is not a source of fungal infections. Current scientific evidence does not support the proposition that human health has been adversely affected by inhaled mycotoxins in home, school, or office environments.

Air Pollution, Indoor↗