I'm not really debating lead vs mono, just having fun with trauma. None of this contradicts your observations and it is really just in case you are interested, not because it contributes meaningfully to the discussion at hand.
To develop a sucking chest wound the hole in the chest wall must be about 66% or larger than the diameter of the trachea. Most entry wounds are not large enough, many exit wounds are. However, sucking chest wounds make breathing ineffective, but hypoxia from this would take several minutes to cause death. Same as hypoxia from simple loss of lung tissue (which would take a greater than 50% loss). The reason chest seals are vented is because most of the time a wound capable of causing a sucking chest wound also vents air back out preventing a tension pneumothorax.
Thoracic trauma (we will assume the heart and aorta are spared as this is a discussion on lungs) can cause death in a few ways. For rapid causes tension pneumothorax (possibly in the setting of tracheal rupture or bronchial rupture) and tension hemothorax (lungs are highly vascular, so hemorrhage is another possibility) come to mind. Most animals probably die from bilateral tension pneumothorax with a double lung shot. The more damage to the lung tissue itself, the faster air can accumulate in the thoracic cavity and the quicker obstructive shock develops from vena cava and cardiac compression. However, the majority of air that causes this likely passes through the trachea to enter the chest cavity.
The collapse of the lungs from the intrapleural pressure results in the undamaged lung becoming significantly smaller and adds to the impression that the lungs just turned to soup.
It is also important to note that there are flaws with trying to attribute death to one mechanism as they have cumulative effects. The loss of intravascular volume from hemorrhage results in earlier vena cava compression and onset of obstructive shock while the loss of lung tissue reduces physiologic reserve at a moment when the body is entering a hypermetabolic stress state and the increased respiratory effort to fuel that state speeds up tension pneumothorax development, Etc.
