Swine production has undergone rapid transformation from family owned operation to a large scale industrial enterprise. Since increasing number of pigs are reared on a large scale in confined buildings, some of the swine barn workers may be employed to work eight hours per day. Swine barn workers suffer from higher incidences of impaired air flow and lung inflammation, which is attributed to high intensity and interrupted exposures to pig barn air. The air in these barns contains gases, dust, microbes and endotoxin with endotoxin being the major suspect as the cause of lung dysfunction. This review attempts to describe the current state of knowledge of incidences and mechanisms of pulmonary dysfunction following exposure to the barn air.

Canada is among the top five pork exporters of the world with a total pork export of 970,000 tons in the year 2004, which translates into cash receipts of $4.2 billion in the year 2004 representing a 25% increase over the year 2003. In 2005, Canada had 14.9 million hogs which is an increase of 1.7% over the previous year and the pork export is expected to grow by 2% [1,2]. Currently, pork sector accounts for 30% of total livestock shipments and for 10% of all farm cash receipts in Canadian farm economy. Further, swine farming has provided employment to 10,790 people in Canada [3]. Therefore, swine production is a major component of Canada's agricultural economy. Although the number of pigs has increased but the number of farms has shown a decline to indicate fewer people are working longer shifts on the farms. Now a days, small family operated pig farms are making way for large scale facilities where thousands of pigs are raised in a single facility [4]. Large pig production operations require many full time workers who work 8 hour/day and 5 days/week and thus experience high intensity interrupted exposures to the barn air [5,6]. However, still many workers may work only a few hours every day inside a pig barn. The barn air is very complex and contains organic dust, plant materials (pollen grains, feed grains, hay and silage), animal origin materials (swine dander, hair, urine and pig proteins), microbial components (mite or their parts, bacteria, endotoxin, (1–3) β-D-glucan and fungal spores) and a number of gases such as ammonia, carbon dioxide, hydrogen sulphide and methane [7-9]. Therefore, although modern barns appear cleaner, the air inside these barns still carries toxic molecules which are harmful to the workers [10].

To better understand the negative effects of exposure to swine barn air, many researchers have exposed naïve, healthy volunteers to the swine barn air for a short period of time (2–5 hours, once). This study model mimics the lung response of new workers following first exposure to the swine barn air. Single two-five hours of exposure of naïve, healthy volunteers to swine barn air is shown to induce bronchial responsiveness [28], fever, malaise and drowsiness [21]. Across the shift change in lung function during exposure is an important predictor of longitudinal changes in lung function in swine confinement workers [29]. Further, a 75-fold increase in neutrophils, a two-three fold increase in mononuclear cells and a significant increase in eosinophils, fibronectin and albumin levels in bronchoalveolar lavage fluid (BALF) [21] and levels of IL-1β, IL-1 receptor antagonist, IL-6 and TNF-α increased in the serum of the exposed naïve volunteers. The changes in IL-1 receptor antagonist levels correlated with changes in FEV1, bronchial responsiveness, oral temperature and white blood cell count while IL-1β levels correlated with oral temperature [30]. Further, it is shown that, a single exposure to barn air also caused thickening of nasal mucosa, increased numbers of neutrophils in nasal lavage and BALF, increased numbers of macrophages, lymphocytes, eosinophils and the levels of IL-8 in the BALF [31,10]. Interestingly, levels of IL-8, a potent chemoattractant for neutrophils, correlated with increase in neutrophils in the nasal lavage fluid [31]. It is obvious that single exposure to the barn air can activate an inflammatory response in human lungs.

Several researchers have shown the inflammatory potential of swine barn dust or air in many in vitro experiments [38-40]. These in vitro studies are a valuable tool to understand the effects of swine barn air or dust on a variety of lung cells. These studies provide an opportunity to control various variables to facilitate identification of cellular and molecular pathways that regulate response to swine barn air. Swine dust induces release of IL-8 in normal human bronchial epithelial cells, human pulmonary epithelial carcinoma cell line (A549) and in human alveolar macrophages [38]. Swine dust is almost as potent as lipopolysaccharides in stimulating cytokine release from alveolar macrophages in vitro [39]. Recent data showed that swine barn dust activates protein kinase C to induce secretion of IL-8 and IL-6 from airway epithelial cells and promotes adhesion of lymphocytes through upregulation of ICAM-1 [40,41]. Swine barn dust can also directly activate T-lymphocytes [42]. These data show importance of performing in vitro studies along with human and experimental animal investigations to further our understanding of lung responses to pig barn air.

The data from animal and human studies show that barn air can induce lung dysfunction. Recent data from animal studies and from in vitro studies have started to elucidate mechanisms of lung dysfunction induced following exposure to the barn air. However, many questions remain unanswered. One of the central questions relates to precise and relative contributions of various toxic molecules in the barn air to lung dysfunction. The endotoxin is the foremost toxic agent in the barn air. The role of endotoxin in barn air induced lung dysfunction can be assessed through the use of mice that lack a functional Toll-like receptor-4. Second logical experiment is the physical and biochemical characterization of the dust particles in the barn air. Specifically, we need to know if the barn air contains dust particles which are less then 100 nm in size because particles of this size are believed to provoke a vigorous cardiopulmonary response [43,44]. The biochemical characterization of the particles would reveal if particles are used as Trojan horse to carry endotoxins and other toxic molecules into the lungs.

The authors declare that they have no competing interests.

Both the authors contributed equally in the preparation of this review.