For asthma, although the search retrieved 3101 papers, only three13–15 reported longitudinal studies in which the incidence of asthma or asthma-associated symptoms in relation to occupation could be found as an outcome Table 1. This is a sparse publication record considering the fact that the percentage of asthma-related disability-adjusted life years (DALY) attributable to workplace exposure remains quite high and closer to the one due to smoking.16 In one of the longitudinal study the authors, during the follow-up period, found an association between occupational exposure to gas, dust and fumes and persistence of asthma, but not an increased incidence of new onset asthma.14 The same authors, in the context of a multicentre national study, suggested a possible role of lifetime occupational exposure to gas, dust and fumes in the persistence/worsening of severe asthma as well.17 Nevertheless, in individuals with occupational asthma, the prevalence of severe asthma was found to be high and often related to a persistent exposure to asthmagens at work.18 Among the new asthmagens, disinfectants may play an important role, as was highlighted by an analysis of the large American nurses’ study included in Table 1, indicating a risk associated with high exposure, even though “no” exposure to disinfectant was statistically associated with incident asthma in the same population.19 In another paper, occupational exposure to extreme cold weather was associated with an increase in the incidence of wheezing.15 In the 2018–2023 period, no systematic review was published on asthma incidence and work-related risk factors. In summary, few relevant publications were published in the study period on incident occupational asthma, even though the importance of work-related exposures regarding asthma control and the socioeconomical impact of work-related asthma is widely appreciated.18 Thus, the need remains for updated scientific evidence on the epidemiological impact of occupational exposure in asthma based on incidence data.

Since the last update of the occupational burden of respiratory diseases few papers were published on asthma. There is a need of updated scientific evidence on the epidemiological impact of workplace exposure on asthma incidence.

The search retrieved 5863 documents for COPD and 2684 for chronic bronchitis. Of these, we identified 12 relevant publications for COPD20–31 and 8 for chronic bronchitis24,28,31–36Tables 2 and 3. The overall results show a slight decrease in risk-estimates compared with previous papers. This could reflect a reduction in exposure to occupational hazards in more recent years or an underestimation of the exposure. In fact, classification of exposure is a very important issue. Studies carried out in the last 5 years confirm the trend to use COPD-specific job exposure matrices instead of self-reported exposure or in-house expert opinion. However, an objective parameter, such as airway obstruction, is less influenced by the risk of a recall bias regarding exposure than a self-reported diagnosis/symptom. Another interesting aspect concerns the interaction between occupational exposure and smoking habits, which was analysed in two studies.26,30 The association between workplace exposure and airway obstruction was clear only in ever-smokers, and this could reflect an interaction between smoking and workplace pollutants, where smoking is needed to prime the inflammation in the airways to allow the noxious effects of workplace pollutants.37 Such an association highlights the relevance of occupational physicians, GP and pulmonologists advising workers exposed to vapours, gases, dusts and fumes (VGDF) or other pollutants to quit smoking. Another interesting finding is the potential role of pesticide exposure as a strong occupational risk factor for airways obstruction.20,28

Yet another important aspect of the recent literature involves the definition of COPD. The most frequent definition of COPD used in epidemiological studies is (fixed) airways obstruction, even in the included studies, although one study used a definition by a pharmacological register (anticholinergic use, a treatment for COPD),29 while in another COPD was “doctor-diagnosed COPD”. Interestingly, in one study,25 the association between COPD and occupational exposure was more obvious using a more clinical definition of COPD, also comprising COPD symptoms besides the presence of airways obstruction, possibly highlighting the presence of a specific, more symptomatic phenotype of COPD, maybe more relevant to occupational exposure risk. The papers included in the Table 2 show that recent publications employ a definition of airflow obstruction based on the lower limit of the normal (LLN) of FEV1/FVC, rather than below the fixed ratio of FEV1/FVC at 0.7. Some recent studies not included in Table 2 took into account the effect of occupational exposure on the crude FEV1/FVC ratio, and in one of these studies, workplace exposure had no effect on lung function;36 this was probably influenced by the fact that the prevalence of the exposure, estimated by an expert panel, was very low compared with similar studies20 and was also lower than the self-reported exposure from the same population.27 In other studies, occupational exposure was associated with a reduction in FEV1/FVC ratio, though not with excess lung function decline in a follow-up period of 4.5 years.38 In addition to the new studies summarized above, multiple reviews of occupational exposure and COPD have been published,39–41 confirming the 2019 ATS/ERS statement findings with an average increased odd of COPD related to occupational exposure ranging between 40 % and 69 % (OR 1.40–1.69).

The same assumptions made for COPD are valid for chronic bronchitis Table 3: for example, the emerging role of pesticide exposure on chronic bronchitis symptoms. Some of the studies24,32,34 used self-reported exposure to occupational pollutants (e.g. dusts, fumes, etc.) as an exposure indicator: in fact, this can be at higher risk of recall bias in subjects with chronic bronchitis symptoms than in healthy subjects. Again, in one study, chronic bronchitis was associated with occupational exposures only in ever smokers, suggesting an interaction between these risk factors in producing airway inflammation and respiratory symptoms such as cough and phlegm.33 Finally, studies with imaging features of COPD and occupational exposure are increasing. In one of these studies, exposure to VGDF was associated with lung CT-scan abnormalities, reflecting a real pulmonary anatomical impairment rather than just symptoms of airflow limitation.42

There is growing evidence of the impact of workplace exposure to vapours, gases, dusts and fumes on COPD and chronic bronchitis occurrence, also in developing countries

The search retrieved 515 articles on the association between occupational exposure and IPF, among which three were case-control studies, meeting our inclusion criteria43–45Table 4. In addition, there was an equal number of newly published systematic reviews on this topic.46–48 This may reflect a growing interest in more definitive diagnostic criteria in light of emerging therapeutic options for IPF.49 The latest evidence confirms the association between dust or second-hand cigarette smoke exposure and IPF. In contrast, asbestos exposure does not seem to be associated with the occurrence of this disease. However, one of the three studies suggested an interaction between asbestos and smoking in increasing the risk of IPF, especially among those having a specific genotype48 and another showed an increased risk of IPF in those who were highly exposed to asbestos.47 Two studies included general population controls, whilst the other considered hospital-based referents. The study carried out in Australia has some characteristics that distinguish it from the other two studies: in particular the sample size was larger, and a specific job exposure matrix (JEM) was used. Interestingly, smoking was not a risk factor in one study46 and it needed the co-exposure with asbestos to be a risk factor in another study.48 Conversely, second-hand cigarette smoke was associated with the occurrence of IPF in all three studies. Finally, duration of exposure to risk factors played an important role strengthening the association between these work-related risk factors and IPF.46

For hypersensitivity pneumonitis (HP) the search identified 252 articles from which five references were cross-sectional studies.50–54Table 5 The prevalence of occupational exposure ranged between 5.8 % and 45.5 %. All the studies were cross-sectional or case-series of HP patients or based on national or local databases of interstitial lung diseases. The exposure was retrieved mainly from information in patient records. In one study52 the classification was based on a positive specific inhalation challenge with occupational antigens. The diagnosis of HP was based on multidisciplinary panel discussion or on single institution's experience. The results were consistent with the findings of the 2019 ATS/ERS statement. In one study, the prevalence of occupational exposure was rather low,50 which may reflect a specific local pattern of exposure, where environmental exposure could be more frequent, as was already reported in the ATS/ERS statement.5 In another study53 the cases attributed to the occupational exposure were only 9.1 %, but in this instance the attribution was made by a positive specific inhalation challenge, which makes it difficult to compare these results with the others. Interestingly, in the time frame considered, a single systematic review on occupational causes of HP was published,55 which included a detailed list of occupational agents that have been associated with HP, in the supplementary material.

The latest scientific evidence confirms an association between occupational exposure to airborne pollutants and IPF or HP, consistent with the findings of the 2019 ATS/ERS statement.

A previous ATS/ERS statement summarised data showing that welders and other workers exposed to metal fumes and inorganic dusts have an increased risk of pneumococcal pneumonia, with the attributable fraction for welders exceeding 50 %5. In the general population, the population attributable fraction for community acquired pneumonia (CAP) was 10 %. We combined a literature search with a narrative approach including original papers, case reports and reviews published in English. Of the 1234 papers retrieved, we identified 28 original papers and three additional papers from the reference lists. Of the 28 original papers, 22 were excluded because of lack of relevant outcome, ambient air pollution, or predictors for vaccinations. The eight publications retained were about pneumococcal pneumonia,56–59 welder's anthrax,60–61 Legionella,62 and Coccidiomycosis.63 We also identified three relevant reviews,64–66 and three case reports.57,67–69

A population-based case-control study of pneumococcal pneumonia found that occupational exposures to inorganic dust, especially silica dust and fumes, including metal fumes, in the year preceding the pneumonia episode increased the disease risk.56 Cumulative exposure further increased the odds for pneumococcal pneumonia.58 Of note, these associations had already been reported in the 1920s.65 Further, working in close contact with other workers, as well as outside work, also increased the risk of pneumococcal pneumonia.59 Clusters of pneumococcal pneumonia cases have been reported in shipyards and construction sites. For example, thirty cases of pneumococcal pneumonia were reported in a shipyard in Finland.67 Most of the cases worked in the docks as plumbers, electricians, welders, or supervisors. Another outbreak involved 20 cases of pneumococcal pneumonia that were reported in a Norwegian shipyard, and most of the patients worked with welding and interior outfitting.68 An outbreak of pneumococcal pneumonia was also detected in a French shipyard.69 The working conditions were described as crowded, with 102 different nationalities and occupational exposures to irritants, metal fumes, dust and chemicals. A subsequent genomic sequencing of outbreak isolates from non-sterile specimen (e.g. nasopharyngeal swab) showed that the Finnish and Norwegian outbreaks were similar, with a common ancestor dated from around 2017.57 Some relevant pathogenetic mechanisms for the increased risk of pneumococcal infections in relation to dust exposure may involve: inorganic dust reducing ciliary beating and initiating overproduction of mucus, which also impairs mucociliary clearance; welding fumes upregulating expression of platelet-activating factor receptor (PAFR) which enhances pneumococcal adherence to epithelial cells; dust particles aiding nutrient acquisition for pneumococci by increasing the permeability of the epithelium thereby augmenting the influx of glucose; and by being filled with dust particles, alveolar macrophages reducing their phagocytosis of pneumococci(possibly the most important mechanism).66

Legionella infections have been described among hotel workers, civil engineering labourers and professional drivers.64 One paper from Japan described three workers who developed Legionella pneumonia when engaged in reconstruction after a period with very heavy rainfall.62 Exposure to infected soil was mentioned as a possible cause of this outbreak.

Seven workers were reported to have an infection caused by an anthrax toxin-expressing Bacillus cereus, and the clinical picture was pneumonia.61 Six of them were welders and one was a metal-worker. Exposure to infected soil was also mentioned as a possible explanation, as most of the cases worked outdoors.

Coccidiomycosis, also known as Valley fever, is caused by inhalation of spores of the fungus Coccidiodes spp, which grows in soil of semi-arid areas.63 Most affected individuals are asymptomatic, but 30–40 % develop fever and a pneumonia-like clinical picture. A cluster of Coccidiomycosis was described among workers constructing solar farms in California.63 Exposures originated from soil-disruptive work, digging and working in trenches.

In conclusion, recent data continue to identify occupational risk factors as potentially important in the prevention of community-acquired pneumonia. The first line of prevention should be reduction of workplace exposures to vapours, gas, dust and fumes. However, despite regulatory activities exposure to dust and fumes may still occur. In such circumstances, it is necessary to provide additional protection by personal respiratory protection. Regarding pneumococcal pneumonia, pneumococcal vaccination should be considered, especially for workers in crowded conditions or with exposure to metal fumes or inorganic dust.

The exposure to occupational pollutants may have an important role in predisposing to infectious pneumonia. For some risk factor (welding fumes) this association is consistent.

Pneumoconiosis, a range of respiratory conditions resulting from occupational inhalation of mineral dusts, remains a persistent global health concern. Inadequate measures to prevent dust exposure, delayed diagnosis, and limited availability of effective treatments contribute to this problem.70 The impact of pneumoconiosis on global health is evident, with substantial new cases and DALYs reported in 2019, particularly in China, where the burden of DALYs attributable to pneumoconiosis is disproportionately high.71,72 While the age-standardised incidence (ASIR) and DALY rates associated with pneumoconiosis have seen a gradual decrease between 1990 and 2019, a notable disparity between genders still remains, with a larger increase in incidence observed in males above the age of 20 years.73,74 There has been an upward trend in ASIRs of Asbestosis, particularly in high-income regions like North America and Australasia.75 These findings highlight the ongoing challenges and regional variations in addressing pneumoconiosis as a global health issue.