Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, diesel exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of diesel exhaust, and especially the particular matter components. Acute effects of diesel exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function. There are also observations supporting the hypothesis that diesel exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, diesel exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response. Much of the research on adverse effects of diesel exhaust, both in vivo and in vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of diesel exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans.

https://erj.ersjournals.com/content/erj/17/4/733.full.pdf

Health effects of diesel exhaust emissions.

Possible mechanisms to explain dust overloading of the lungs

pReVIously ClAssIfIed by IARC As “CARCInogenIC to humAns (gRoup 1)” And wAs deVeloped by sIx sepARAte woRkIng gRoups: phARmACeutICAls; bIologICAl Agents; ARsenIC, metAls, fIbRes, And dusts; RAdIAtIon; peRsonAl hAbIts And IndooR CombustIons; ChemICAl Agents And RelAted oCCupAtIons. thIs Volume 100f CoVeRs ChemICAl Agents And RelAted oCCupAtIons, speCIfICAlly 4-AmInobIphenyl, benzIdIne, dyes metAbolIzed to benzIdIne, 4,4’-methylenebIs(2-ChloRoAnIlIne), 2-nAphthylAmIne, oRtho-toluIdIne, AuRAmIne And AuRAmIne pRoduCtIon, mAgentA And mAgentA pRoduCtIon, benzo[A]pyRene, CoAl gAsIfICAtIon, oCCupAtIonAl exposuRes duRIng CoAl-tAR dIstIllAtIon, CoAl-tAR pItCh, Coke pRoduCtIon, untReAted oR mIldly tReAted mIneRAl oIls, shAle oIls, soot, As found In oCCupAtIonAl exposuRe of ChImney-sweeps, oCCupAtIonAl exposuRes duRIng AlumInIum pRoduCtIon, AflAtoxIns, benzene, bIs(ChloRomethyl)etheR And ChloRomethyl methyl etheR, 1,3-butAdIene, 2,3,7,8-tetRAChloRodIbenzo-pARA-dIoxIn, 2,3,4,7,8-pentAChloRodIbenzofuRAn, And 3,3’,4,4’,5-pentAChloRobIphenyl, ethylene oxIde, foRmAldehyde, sulfuR mustARd, VInyl ChloRIde, IsopRopyl AlCohol mAnufACtuRe by the stRong-ACId pRoCess, mIsts fRom stRong InoRgAnIC ACIds, oCCupAtIonAl exposuRes duRIng IRon And steel foundIng, oCCupAtIonAl exposuRe As A pAInteR, oCCupAtIonAl exposuRes In the RubbeR mAnufACtuRIng IndustRy. beCAuse the sCope of Volume 100 Is so bRoAd, Its monogRAphs ARe foCused on key InfoRmAtIon. eACh monogRAph pResents A desCRIptIon of A CARCInogenIC Agent And how people ARe exposed, CRItICAl oVeRVIews of the epIdemIologICAl studIes And AnImAl CAnCeR bIoAssAys, And A ConCIse ReVIew of the Agent’s toxICokInetICs, plAusIble meChAnIsms of CARCInogenesIs, And potentIAlly susCeptIble populAtIons, And lIfe-stAges. detAIls of the desIgn And Results of IndIVIduAl epIdemIologICAl studIes And AnImAl CAnCeR bIoAssAys ARe summARIzed In tAbles. shoRt tAbles thAt hIghlIght key Results ARe pRInted In Volume 100, And moRe extensIVe tAbles thAt InClude All studIes AppeAR on the monogRAphs pRogRAmme websIte (http://monogRAphs.IARC.fR). It Is hoped thAt thIs Volume, by CompIlIng the knowledge ACCumulAted thRough seVeRAl deCAdes of CAnCeR ReseARCh, wIll stImulAte CAnCeR pReVentIon ACtIVItIes woRldwIde, And wIll be A VAlued ResouRCe foR futuRe ReseARCh to IdentIfy otheR Agents suspeCted of CAusIng CAnCeR In humAns. D es ig n by A ude la d es m ot s

iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns

Damp buildings often have a moldy smell or obvious mold growth; some molds are human pathogens. This has caused concern regarding health effects of moldy indoor environments and has resulted in many studies of moisture- and mold-damaged buildings. Recently, there have been reports of severe illness as a result of indoor mold exposure, particularly due to Stachybotrys chartarum. While many authors describe a direct relationship between fungal contamination and illness, close examination of the literature reveals a confusing picture. Here, we review the evidence regarding indoor mold exposure and mycotoxicosis, with an emphasis on S. chartarum. We also examine possible end-organ effects, including pulmonary, immunologic, neurologic, and oncologic disorders. We discuss the Cleveland infant idiopathic pulmonary hemorrhage reports in detail, since they provided important impetus for concerns about Stachybotrys. Some valid concerns exist regarding the relationship between indoor mold exposure and human disease. Review of the literature reveals certain fungus-disease associations in humans, including ergotism (Claviceps species), alimentary toxic aleukia (Fusarium), and liver disease (Aspergillys). While many papers suggest a similar relationship between Stachybotrys and human disease, the studies nearly uniformly suffer from significant methodological flaws, making their findings inconclusive. As a result, we have not found well-substantiated supportive evidence of serious illness due to Stachybotrys exposure in the contemporary environment. To address issues of indoor mold-related illness, there is an urgent need for studies using objective markers of illness, relevant animal models, proper epidemiologic techniques, and examination of confounding factors.

http://dzumenvis.nic.in/microbes and plants growth/pdf/indoor mold, toxigenic fungi.pdf

Indoor Mold, Toxigenic Fungi, and Stachybotrys chartarum: Infectious Disease Perspective

Health effects of ambient air pollution in children

Carbon black aerosols were used as a probe of the pulmonary retention and clearance of submicron particles. Male Fischer rats (COBS CD) were exposed for 20 h/d, 7 d/wk for 1, 3, or 6 wk to either 7 ± 2 mg/m3 carbon black or filtered air. The submicron aerosol (mass median aerodynamic diameter, MMAD, 0.24 μm) was generated with a Wright dust feed‐cyclone system. Lung and hilar lymph node particle burdens were determined immediately following the exposure and at preselected intervals up to 1 yr postexposure. After 1‐, 3‐, and 6‐wk exposures, the lung burdens were 1.1 ± 0.1, 3.5 ± 0.2, and 5.9 ± 0.1 mg, respectively. One year after a 1‐, 3‐, or 6‐wk exposure, 8%, 46%, and 61% of the initial lung burden remained in the lungs. Initially, the hilar lymph nodes contained 0.2%, 0.9%, and 2.0% of the lung burdens in the 3 exposure groups, respectively. At 1 yr postexposure, particle translocation from the lungs led to a rise in lymph node burdens to 1%, 21%, and 27% of the initial lung burden. The retention of car...

Retention and clearance of inhaled submicron carbon black particles

Inhalation exposures to diluted diesel exhaust were conducted in F344 rats for the last five years to enable a better understanding of lung clearance of inhaled diesel particles (DP). We observed that as the DP burden in the lungs increased, lung clearance decreased and the extent of particle-laden macrophage aggregation in the alveoli increased. A new compartmental model of particle retention in the lungs was developed by treating the macrophage aggregates as a particle sequestering compartment. Features of the model are non-linear compartmental clearance of particulate and a mass-dependent transition from elimination to sequestration of particulate in the lungs. A new experimental exposure for 12 weeks to 6 mg DP/m³ was conducted to collect data to test the predictions of the model and to be used later in refining the rate coefficients of the model. This report shows that there is good agreement between the data and the predicted lung and lymph node burdens.

Pulmonary Retention of Inhaled Submicron Particles in Rats: Diesel Exhaust Exposures and Lung Retention Model

A tunable impedance load bearing structure includes a support comprising an active material configured for supporting a load, wherein the active material undergoes a change in a property upon exposure to an activating condition, wherein the change in the property is effective to change an impedance characteristic of the support.

Tunable impedance load-bearing structures

Particulate material in diesel engine exhaust deposits in the lungs of exposed animals. A technique for measuring the amount of soot in the lungs would be useful for determining the rates of the deposition and clearance of the submicron particles. The paper describes the use of light extinction for quantitating diesel particles in aqueous suspension. Particles collected by electrostatic precipitation and finely suspended in 0.01 N NaOH by sonication strongly absorb visible light. The extinction of light at 750 nm is proportional to the mass concentration of particles, with an extinction coefficient of 28 +/- 1 cm2 mg-1. Lungs from guinea pigs exposed to dilute diesel exhaust were dried and digested in potassium hydroxide and ethanol. The insoluble particles were centrifuged and resuspended in water by sonication. The optical density of the suspension was compared to that of suspensions made from lungs of animals not exposed to diesel exhaust, with or without known amounts of particulate added at the beginning of digestion. A concentration-dependent increase in the total amount of particles per lung was found for guinea pigs exposed to 0, 269, 813 and 1530 micrograms m-3 diesel particles for 6 months.

A spectrophotometric method for the quantitation of diesel exhaust particles in guinea pig lung

Rats were exposed to three concentrations of diluted diesel exhaust for 6 mo and 1 yr. Bronchopulmonary lavage was used to obtain the pulmonary phagocytes from the animals in order to study the response of the phagocytic defenses to the inhaled particulate. The cell numbers and volumes were measured using an electronic particle counter. The cell counts of alveolar macrophages (AM) were proportional to the concentration of diesel exhaust particulate (DP) in the chronic exposures. AM increased in the lungs in response to the rate of DP mass entering the lungs, rather than to the total DP burden in the lung. The geometric mean volumes of AM from the exposed and control animals were approximately 1100 micron3 at both 6 and 12 mo of exposure, although exposed cell-volume distributions skewed towards larger sizes. The AM volume distributions extended to 2000 micron3 in both control and 250 micrograms DP/m3 exposed animals and up to 5000 micron3 in cells from animals exposed to 750 and 1500 micrograms DP/m3. The volume distributions were found to be reproducible in equivalent control and exposed cell populations. Polymorphonuclear leukocytes were present in the lavaged cell populations from the animals exposed to 750 and 1500 micrograms/m3. In addition, at 1 yr of exposure, lymphocytes were also lavaged from animals exposed to 750 and 1500 micrograms DP/m3. Protein, beta-glucuronidase activity, and acid phosphatase activity were measured in the lavaged cells, and were elevated in the cells from animals exposed to 750 and 1500 micrograms/m3. The buoyant density of diesel-laden AM was found to be greater than that of control AM, and overlapped with the buoyant density of the polymorphonuclear leukocytes.

Kenneth A. Strom

Papers

Retention and clearance of inhaled submicron carbon black particles

Pulmonary Retention of Inhaled Submicron Particles in Rats: Diesel Exhaust Exposures and Lung Retention Model

Tunable impedance load-bearing structures

A spectrophotometric method for the quantitation of diesel exhaust particles in guinea pig lung

Response of pulmonary cellular defenses to the inhalation of high concentrations of diesel exhaust.