A 35-year-old male with a history of smoking since he was 16 years old (8-10 cigarettes/day) and employed for about 2 years in a fireproofing company processing paint and rock wool (material with high silica content). The patient reports working with machines that grind rock wool and project dust, so exposure to this material is constant. He also reports previous episodes of rhinorrhea with the expulsion of black soot for two days. He has been experiencing exertional dyspnea for a year and a weight loss of 6 kg during this period. Subsequently, due to exacerbation of dyspnea and respiratory difficulty, he was referred to external pulmonology consultations. He has no other relevant medical history, does not have pets, nor does he engage in related activities. On physical examination, he presented with a blood pressure of 121/79 mmHg, heart rate of 84 bpm, arterial blood gas with an O2 saturation of 92%, and an inspired oxygen fraction (FiO2) of 0.21. Additionally, exertional dyspnea was identified without cough, expectoration, fever, or thermal sensation, and no orthopnea. The patient reports occasional apneas with some asphyctic awakenings. The tests to evaluate the respiratory function, including forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and FEV1/FVC ratio were normal. On laboratory analysis, increased levels of lactate dehydrogenase (LDH) of 530 mg/dL (RI: 210-425 mg/dL) and angiotensin converting enzyme (ACE) of 75 U/L (RI: 20-70 U/L) were observed. The chest X-ray and high-resolution computed tomography (HRCT) revealed diffuse bilateral lung involvement with a ground-glass pattern and smooth thickening of the interlobular septa, adopting a paving stone pattern with a tendency to consolidation in the posterior region of the middle third of the left inferior lobe and. The rest of the blood and urine tests were normal, including complete blood count, coagulation, antinuclear antibodies (ANA), and antineutrophil cytoplasmic antibodies (ANCA), complete biochemistry with liver, renal, and bone metabolism functions. Moreover, microbiological results were negative for Gram staining, fungal cultures, and PCR for Adenovirus (A, B, C, D, and E), Parainfluenza virus (1, 2, 3, and 4), Rhinovirus (A, B, and C), Influenza A and B viruses, Metapneumovirus, Aspergillus, Pneumocystis jirovecii, and Mycobacteria. With these findings, a differential diagnosis was raised between: alveolar proteinosis (primary or secondary to rock wool inhalation) as the first possibility, or less likely sarcoidosis (no lymph node or pleural involvement), lipoid pneumonia (no areas of fatty density observed, and the involvement was extensive), infectious origin (bacterial, viral, and P. jiroveci cultures were negative), or bronchioalveolar carcinoma. After discussing the case with the immunology service, determination of anti-GM-CSF antibodies was requested due to suspicion of primary PAP, and the results were positive with a figure of 8.2 U/mL (Rl: <5 U/mL). The determination of anti-GM-CSF antibodies was performed using a ClinMax™ Human GM-CSF Quantitative ELISA kit, which is a standard sandwich immunoassay designed to quantify GM-CSF present in complex biological matrices such as human serum, plasma, and buffer solution. Additionally, the patient underwent a transbronchial biopsy in the left inferior lobe, and the samples were sent to the Pathology Department. The histological studies of the lung biopsy confirmed the diagnosis of PAP. Based on the clinical, analytical, radiological, and anatomopathological findings, the patient was diagnosed with primary pulmonary alveolar proteinosis (PAP). The secondary origin could not be demonstrated due to the absence of previous sera to determine anti-GM-CSF concentrations. Combined treatment was decided upon, consisting of bronchoalveolar lavage (BAL) techniques along with nebulized sargramostim administration.