Bronchoalveolar Lavage as a Diagnostic Window into Human Exposure to Microplastics and Associated Lung Changes

Abstract

Background:

Microplastics are emerging airborne pollutants increasingly implicated in respiratory health risks. Although ingestion has been widely studied, inhalation of microplastics and their potential pulmonary impact remain underexplored. Bronchoalveolar lavage (BAL) provides a minimally invasive diagnostic technique for detecting inhaled particles and assessing associated inflammatory changes.

Methods:

This cross-sectional study was conducted among 60 adult patients undergoing diagnostic bronchoscopy for non-infective pulmonary complaints. BAL fluid was collected and filtered to detect microplastics using polarized light microscopy and Fourier-transform infrared (FTIR) spectroscopy. Cytological examination and cytokine analysis (IL-6, TNF-α) were also performed. Data were statistically analyzed using SPSS v25, with significance set at P < 0.05.

Results:

Microplastics were detected in 70% of BAL samples, with polyethylene and polypropylene being the most common types. The mean microplastic count was 6.4 ± 3.1 particles per 100 mL BALF. Individuals with detectable microplastics showed significantly higher macrophage (65.4% vs. 58.6%, P = 0.012) and neutrophil (18.2% vs. 12.4%, P = 0.003) percentages in BAL cytology, alongside elevated IL-6 and TNF-α levels (P < 0.001). Lymphocyte proportions were relatively lower in exposed individuals (P = 0.017).

Conclusion:

Bronchoalveolar lavage is a valuable tool for detecting pulmonary microplastic exposure and related inflammatory changes. These findings underscore the potential health risks posed by airborne microplastics and support the need for environmental and occupational health interventions.

INTRODUCTION

Microplastics—plastic particles less than 5 mm in diameter—have emerged as ubiquitous environmental pollutants with increasing concern regarding their impact on human health. While initial research has primarily focused on marine ecosystems and ingestion through food and water, growing evidence suggests that inhalation of airborne microplastics represents a significant and underrecognized route of human exposure, particularly in urban and industrial environments.[1]

The respiratory system is highly vulnerable to particulate pollutants due to its large surface area and continuous exposure to inhaled air. Inhaled microplastics may deposit in the lower respiratory tract, inducing local inflammation, oxidative stress, and potentially fibrotic remodeling.[2] Studies in animal models have shown that microplastic exposure leads to histological changes such as alveolar thickening, macrophage activation, and even granuloma formation.[3] However, data on human pulmonary exposure and tissue-level responses remain scarce.

Bronchoalveolar lavage (BAL), a minimally invasive diagnostic technique, allows for the collection of cells and soluble components from the lower respiratory tract. BAL fluid analysis has been instrumental in studying various inhalational lung diseases, including those associated with occupational and environmental exposures. As such, BAL provides a unique and valuable window into detecting and characterizing microplastic particles within the lung microenvironment.

This study explores the utility of bronchoalveolar lavage in identifying microplastics and evaluating associated cytological and histopathological changes in the lungs, aiming to bridge a critical gap in current understanding of microplastic-related pulmonary toxicity.

METHODS

This cross-sectional, hospital-based study was conducted over a 12-month period at a tertiary care center specializing in pulmonary medicine. Ethical approval was obtained from the institutional ethics committee, and informed written consent was secured from all participants.

The study included 60 adult patients undergoing diagnostic bronchoscopy with bronchoalveolar lavage (BAL) as part of clinical evaluation for non-infective respiratory symptoms such as chronic cough, dyspnea, or unexplained radiological opacities. Patients with known lung malignancies, active infections, or prior thoracic surgeries were excluded to eliminate confounding factors.

Sample collection

BAL was performed using flexible fiberoptic bronchoscopy under local anesthesia and conscious sedation. A total of 100-150 mL of sterile saline was instilled in aliquots into the right middle lobe or lingula and gently aspirated back. The recovered BAL fluid (BALF) was collected in sterile containers and immediately processed.

Microplastic detection and characterization

BALF samples were filtered through 0.45 µm pore-sized membranes and digested enzymatically to remove organic debris. Filter membranes were examined under polarized light microscopy to detect birefringent microplastic particles. Suspected particles were further analyzed using Fourier-transform infrared (FTIR) spectroscopy for polymer identification.

Cytological and inflammatory markers

Cytospin smears were prepared for differential cell counts (macrophages, lymphocytes, neutrophils, eosinophils). Inflammatory cytokines (e.g., IL-6, TNF-α) were measured in BALF supernatants using ELISA.

Data analysis

Statistical analysis was conducted using SPSS v25. Descriptive statistics were used for demographic and exposure variables. Associations between microplastic burden and inflammatory markers or cytological findings were analyzed using Pearson correlation and independent t-tests. A P value < 0.05 was considered statistically significant.

RESULTS

Out of 60 participants, microplastics were detected in 70% (n = 42) of BALF samples, confirming significant pulmonary exposure. Polyethylene (PE) was the most commonly identified polymer (57.1%), followed by polypropylene (42.8%) and polystyrene (23.8%). The mean particle count among positive cases was 6.4 per 100 mL of BAL fluid [Tables 1 and 2].

Table 1.

Baseline demographic and clinical characteristics (n=60)

Characteristic		Value
Mean age (years)		46.8±11.4
Gender (M:F)		38:22
Mean BMI (kg/m2)		24.6±3.2
Smoking status		35 (58.3%) current/former
Occupational exposure*		26 (43.3%)
Chronic respiratory symptoms (>3 months)		41 (68.3%)

*Significant

Table 2.

Microplastic detection and types in BALF samples

Parameter		Frequency (%)
Microplastics detected (any type)		42 (70.0%)
No microplastics detected		18 (30.0%)
Mean particle count (per 100 mL BALF)		6.4±3.1
Types of microplastics identified:
– Polyethylene (PE)		24 (57.1%) of 42
– Polypropylene (PP)		18 (42.8%) of 42
– Polystyrene (PS)		10 (23.8%) of 42
– Mixed/other		5 (11.9%) of 42

Patients with detectable microplastics demonstrated significantly elevated neutrophil and macrophage counts in BAL cytology, indicating an active inflammatory response. Conversely, lymphocyte proportions were lower, suggesting a shift toward innate immune activation. Cytokine analysis showed markedly higher IL-6 and TNF-α levels in microplastic-positive individuals compared to those without detectable particles (P < 0.001), supporting a link between microplastic exposure and pro-inflammatory lung activity [Table 3].

Table 3.

BAL cytology and inflammatory markers by microplastic presence

Parameter		Microplastic present (n=42)		No microplastic (n=18)		P
Macrophages (%)		65.4±8.2		58.6±7.9		0.012*
Neutrophils (%)		18.2±5.6		12.4±4.7		0.003*
Lymphocytes (%)		12.1±3.4		15.8±4.1		0.017*
IL-6 (pg/mL)		34.5±11.3		19.8±8.4		<0.001*
TNF-α (pg/mL)		28.9±9.1		16.7±6.9		<0.001*

*Significant

DISCUSSION

This study provides novel evidence supporting the use of bronchoalveolar lavage (BAL) as a diagnostic tool for detecting inhaled microplastics and assessing their associated pulmonary effects. The detection of microplastics in 70% of BALF samples highlights the high burden of environmental exposure, even among non-industrial populations, likely due to increasing urban pollution and indoor air contamination.[1,4]

The predominant presence of polyethylene (PE) and polypropylene (PP)—commonly used in packaging and textiles—is consistent with previous studies that have identified these polymers in atmospheric fallout and household dust.[5,6] The mean microplastic burden of 6.4 particles per 100 mL BALF aligns with earlier autopsy-based studies that demonstrated plastic fibers embedded in human lung tissue.[7] However, the present study is one of the first to document this via a minimally invasive, in vivo approach.

The cellular response to microplastic exposure was characterized by elevated macrophage and neutrophil counts in BAL fluid, suggesting activation of innate immune pathways. These findings are corroborated by experimental models showing that inhaled microplastics trigger oxidative stress, phagocytic activity, and pro-inflammatory cytokine release in alveolar macrophages.[8] Our results demonstrated significantly higher levels of IL-6 and TNF-α in exposed individuals, indicating a sustained inflammatory milieu within the lower respiratory tract—factors known to contribute to chronic lung pathology, including fibrosis and asthma-like changes.

Interestingly, we also observed a relative reduction in lymphocytes in the BAL of microplastic-positive cases, which may reflect a suppression of adaptive immune elements or a compensatory redistribution during acute inflammation. This immune imbalance warrants further investigation to understand long-term consequences.

CONCLUSION

These findings highlight the utility of BAL not only for direct microplastic detection but also for characterizing the pathophysiological landscape induced by these novel pollutants. Given the growing recognition of microplastic toxicity, especially in occupational and urban settings, there is an urgent need for environmental regulations, protective guidelines, and continued clinical surveillance of at-risk populations.

Conflict of interest

Nil.

Funding Statement

Nil.